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Transcript
Volume 14 Issue 2 Summer 2015
The International
Student Journal
of Nurse Anesthesia
TOPICS IN THIS ISSUE
Negative Pressure Pulmonary Edema
Robotic-Assisted Cystoprostatectomy
General Anesthesia in the Parturient
Acute Intermittent Porphyria
Accidental Dural Puncture
Supraorbital Hematoma
Cri du Chat Syndrome
Mitral Valve Prolapse
Myasthenia Gravis
ACE inhibitors
TIVA for MH
High Spinal
INTERNATIONAL STUDENT JOURNAL OF NURSE ANESTHESIA
Vol. 14 No. 2 Summer 2015
Editor
Vicki C. Coopmans, CRNA, PhD
Associate Editor
Julie A. Pearson, CRNA, PhD
Editorial Board
Laura Ardizzone, CRNA, DNP
Memorial Sloan Kettering Cancer Center; NY, NY
MAJ Sarah Bellenger, CRNA, MSN, AN
Darnall Army Medical Center; Fort Hood, TX
Laura S. Bonanno, CRNA, DNP
Carrie C. Bowman Dalley, CRNA, MS
LTC Denise Cotton, CRNA, DNAP, AN
Janet A. Dewan, CRNA, PhD
Kären K. Embrey CRNA, EdD
Rhonda Gee, CRNA, DNSc
Marjorie A. Geisz-Everson CRNA, PhD
Robert Hawkins, CRNA, MBA, DNP
Johnnie Holmes, CRNA, PhD
Donna Jasinski, CRNA, DNSc
Ilene Klassy, CRNA, MSN
Connie L. Lorette, CRNA, PhD
Johanna Newman, CRNA , DNAP
Greg Nezat, CRNA, PhD
Teresa Norris, CRNA, EdD
Justice Parrott, CRNA, DNAP
Shannon Pecka, CRNA, PhD
Sarah Perez, CRNA, MS, MSN
Jo Ann Platko, CRNA, BC, PhD
Michael Rieker, CRNA, DNP, FAAN
Dennis Spence, CRNA, PhD
Bryan Tune, CRNA, DNP
Maria Van Pelt, CRNA, MS, MSN
Kelly Wiltse Nicely, CRNA, PhD
Lori Ann Winner, CRNA, MSN
Kathleen R. Wren, CRNA, PhD
Louisiana State University Health Sciences Center
Georgetown University
Winn Army Community Hospital; Fort Stewart, GA
Northeastern University
University of Southern California
Millikin University and
Decatur Memorial Hospital
University of Southern Mississippi
Naval Medical Center; Portsmouth, VA
Uniformed Services University
Georgetown University
University of Wisconsin Medical School
& Medical Foundation
Northeastern University
Florida International University
Naval Hospital; Camp Lejeune, NC
University of Southern California
Uniformed Services University
Bryan College of Health Sciences
Washington University School of Medicine;
Barnes-Jewish College
Somnia Anesthesia, Inc.
Wake Forest Baptist Health
Naval Medical Center; San Diego
National University
Massachusetts General Hospital
University of Pennsylvania
University of Pennsylvania
Arkansas State University
Contributing Editors For This Issue
Barbara Brown, CRNA, MSN
Courtney Brown, CRNA, PhD
Kevin Buettner, CRNA, PhD
Megan Ginter, CRNA, MSNA
Cathy Horvath, CRNA, MSN
Phyllis McCutchen, CRNA, MSN
Art Shimata CRNA MAE
Denise Tola, CRNA, MSN
Wake Forest Baptist Health
Wake Forest Baptist Health
University of North Dakota
Newman University
Georgetown University
Wake Forest Baptist Health
Westminster College
Georgetown University
Reviewers For This Issue
Jennifer E. Badeaux, CRNA, DNP
Raymond Bonds, CRNA, DNP
Shelli Collins, CRNA, MSN
Stephanie Fan, CRNA, MSN
Louisiana State University; Health Sciences Center
Uniformed Services University
Excel Anesthesia, PA; Dallas, TX
Washington University School of Medicine;
St. Louis, MO
Oakland University-Beaumont
Naval Medical Center; Portsmouth, VA
Albany Medical College
Winn Army Community Hospital; Fort Stewart, GA
Texas Christian University
Columbia University
Washington University School of Medicine
University of Wisconsin Medical School
& Medical Foundation
Lehigh Valley Anesthesia Services; Allentown, PA
Kaiser Permanente School of Anesthesia
Washington University School of Medicine;
Barnes-Jewish College
Darnall Army Hospital; Fort Hood, TX
Union University
Washington University School of Medicine
Anne Marie Hranchook, CRNA, DNP
John Litchfield, CRNA, PhD
Giovanna Mahar, CRNA, MS
MAJ Gregg Phillips, CRNA, MSN
J. Dru Riddle, PhD, DNP, CRNA
Cliff Roberson, CRNA, DNP
Mike Rybak, CRNA, MSN
Erin Sebens, CRNA, MS
Maria D. Motovidlak Thomas, CRNA, BA, BS, MSN
Jennifer L. Thompson, CRNA, DNP
Brian Torres, CRNA, MSN
CPT Tina Williams, CRNA, MSN
Molly Wright, CRNA, DNP
Mary Ellen Zerlan, CRNA, DNP
The opinions contained in this journal are those of the authors and do not necessarily represent the opinions of the
program or the University.
Disclaimer for all articles authored by military personnel:
The views expressed in this journal are those of the authors and do not necessarily reflect the official policy or
position of their respective Military Department, Department of Defense, nor the U.S. Government. The work was
prepared as part of the official duties of the military service member. Title 17 U.S.C. 105 provides that ‘Copyright
protection under this title is not available for any work of the United States Government’. Title 17 U.S.C. 101
defines a United States Government work as a work prepared by a military service member or employee of the
United States Government as part of that person’s official duties.
2
Front Cover:
Pictured above, Felicia Anderson, RN, BSN, a graduate student enrolled in the Westminster College nurse
anesthesia program (NAP) provides anesthesia in the program's high-fidelity simulated operating room.
Pictured below, Art Shimata, CRNA, MAE, professor for the Westminster College NAP works with Dan
Bunker, CRNA, MSNA, new assistant professor and alumnae of the Westminster NAP, in the program's
simulation laboratory to plan instruction on ultrasound-guided nerve blocks.
The Guide for Authors: can be found at www.aana.com by following this path:
CE & Education  Students  Scroll down to lower right, click on Student Journal
Or, use this direct link: http://www.aana.com/studentjournal
Table of Contents
3
Case Reports
Perioperative Hematoma Formation following Supraorbital Craniotomy ..............................6
Amrutha Panakkal, University of Pennsylvania
Acute Intermittent Porphyria .......................................................................................................9
Kristal Barbee, Georgetown University
Total Intravenous Anesthesia for Malignant Hyperthermia ...................................................12
Michelle Marciano, Georgetown University
High Spinal in a Morbidly Obese Patient ..................................................................................15
Verity Caruso, Westminster College
Anesthetic Management of a Patient with Myasthenia Gravis ...............................................19
Camille Y. Higdon, Wake Forest Baptist Health
Bradycardia during Robotic-Assisted Cystoprostatectomy.....................................................22
Carolyn C. Hartle, Wake Forest Baptist Health
Preoperative ACE inhibitor use and Refractory Hypotension ................................................25
Stephanie L. Anderson, Wake Forest Baptist Health
Anesthetic Management of Mitral Valve Prolapse ...................................................................29
Jason E. Goodin, Wake Forest Baptist Health
Converting to General Anesthesia in a Complex Parturient ...................................................32
Michael Murphy, Northeastern University
Negative Pressure Pulmonary Edema in a Pediatric Patient...................................................35
Christine DePasquale Calder, Northeastern University
Anesthetic Implications for a Patient with Gitelman’s Syndrome ..........................................39
Jamie Greicar, University of North Dakota
Anesthetic Considerations a for Patient with Cri du Chat Syndrome....................................43
Katie Carmer, Newman University
Evidence-based Practice Analysis Reports
Managing Accidental Dural Punctures with Spinal Catheters................................................46
Tyler Borne, Louisiana State University Health Sciences Center
4
Editorial ........................................................................................................................................53
Vicki C. Coopmans, CRNA, PhD
Guide for Authors ........................................................................................................................54
Perioperative Hematoma Formation following Supraorbital Craniotomy
5
Amrutha Panakkal, MSN
University of Pennsylvania
Keywords: supraorbital craniotomy, perioperative hematoma, nasopharyngeal osteosarcoma
The endoscopic supraorbital approach to craniotomy has changed the amount of exposure needed to
operate on tumors located at the cranial base. Complications such as transient supraorbital nerve injury,
cerebrospinal fluid leak, rhinorrhea and pseudomeningocele formation are known risks.1 However, less
well documented is the formation of a hematoma during the perioperative or immediate postoperative
period, which may arise from prolonged surgery via the supraorbital route. Hematoma formation around
the orbit must be rapidly identified and treated in order to prevent permanent damage to the globe and
optic nerve.
Case Report
A 31-year-old, 165 cm, 66 kg male presented for resection of a right skull base nasopharyngeal
osteosarcoma via supraorbital craniotomy. His medical history included essential hypertension,
nasopharyngeal cancer, right cranial nerve VI compressive neuropathy and cerebrovascular accident
(CVA) three years prior with no residual extremity weakness. His past surgical history included a
percutaneous gastrostomy insertion post CVA that was not associated with any anesthetic complications.
His current medication regimen included dexamethasone and hydrochlorothiazide.
Pre-operative airway evaluation identified a Mallampati classification III, a thyromental distance less
than 6 cm, an inter-incisor distance less than 4 cm, intact dentition, and narrow neck with full range of
motion predicting a difficult airway. The anesthesia team planned an awake fiberoptic intubation to
secure the airway for the procedure.
In the pre-operative area, intravenous (IV) access was established and the patient’s oral and
hypopharynx was topicalized with 4% lidocaine jelly 5 mL applied to a gauze-wrapped tongue
depressor. The patient was brought into the operating room (OR) and standard American Society of
Anesthesiologists monitors were applied with oxygen supplementation at 5 L/min via a nasal cannula.
Midazolam 2 mg IV was administered for anxiolysis and a 7.0 mm cuffed endotracheal tube (ETT) was
passed through the larynx using a pediatric fiberoptic scope following an unsuccessful attempt with an
8.0 mm cuffed ETT. Once end-tidal carbon dioxide (ETCO2) was confirmed and bilateral breath sounds
were noted, anesthesia was induced with propofol 200 mg, rocuronium 30 mg and dexamethasone 10
mg were administered IV. General anesthesia was maintained with Sevoflurane 1.8 – 2.2% inspired
concentration in a mixture of oxygen 1 L/min and air 1 L/min.
The surgical procedure was uneventful. Upon conclusion of the five hour case, neuromuscular blockade
was antagonized with neostigmine 3 mg and glycopyrolate 0.5 mg IV. When the patient was able to
maintain a head lift for >5 seconds, had a + 5 hand grip with bilateral upper extremities and consistently
inspired tidal volumes greater than 400 ml, the ETT was removed.
Following extubation, blood began to ooze from his right eye socket and a hematoma was noted which
6
continued to develop over time. The anesthetic team titrated midazolam 1 mg IV and fentanyl 75 mcg
IV to the patient’s comfort while maintaining a patent airway. Prior to extubation, a total of
hydromorphone 1 mg and fentanyl 250 mcg was administered throughout the case. The surgeon
immediately identified, assessed, and evacuated the hematoma. An ophthalmologist was consulted to
assess the patient’s eyesight in the OR. The patient’s vision was determined intact and he was
transported to post-anesthesia care unit (PACU). In the PACU and throughout his hospital stay, the
patient did not have any further deterioration of sight in his right eye.
Discussion
The supraorbital endoscopic approach to craniotomy is characterized as the keyhole principle, a small
incision that allows wide access to deeper surgical lesions without the need for fixed brain retraction.1
Prior to the supraorbital endoscopic approach, the “cranio-orbito-zygomatic” or “bifrontal approach”
was used for tumors at the cranial base.2,3 These craniotomies required prolonged retraction of the
frontal lobes and an incision that involved the forehead and scalp.2,3,4 The supraorbital endoscopic
approach is being increasingly favored by neurosurgeons because it decreases the amount of trauma to
the patient and provides increased exposure for surgery.3,5 This approach has also become cosmetically
appealing to patients.4 Although the incision is small, there remain complications associated with this
minimally invasive approach.
In order to avoid injury to the neural and vascular structures around the supraorbital incision site, an indepth knowledge of anatomic landmarks is required.2 Complications are very rare in this type of
craniotomy, but some of the potential complications discussed in the literature are transient forehead
numbness, transient frontalis weakness, pseudomeningocele and cerebrospinal fluid (CSF) rhinorrhea.3
Damage to the supraorbital nerve is the cause of transient forehead numbness and it is one of the
common complications in the early postoperative period.3 Transient frontalis weakness from injury,
which is caused by stretching of the frontalis branch of the facial nerve, can also be seen immediately
after surgery.3 Both transient forehead numbness and transient frontalis weakness are related to the soft
tissue dissection and retraction of surgery.3
Pseudomeningocele can occur when CSF collects in the pocket of space created over the frontal bone
and CSF rhinorrhea may occur if the frontal sinus is interrupted or inadequately repaired.3 If the patient
develops CSF rhinorrhea postoperatively and requires immediate repair of the leak, anesthesia providers
need to be cautious in providing positive pressure mask ventilation during induction, as this might cause
pneumocephalus.1 Additionally, a pneumocephalus may also occur when positive pressure is present in
the upper airway, as with an airway obstruction, because air can be forced “into the skull through any
openings of the facial bone.”1
Smooth emergence is critical in endoscopic supraorbital craniotomies due to the increased risk of
pneumocephalus and also pseudomeningocele.1 Applying gentle pressure over the surgical site during
extubation can decrease the incidence of these potential complications.3 During supraorbital approach
craniotomy the anesthesia provider has limited access to the airway as the operating table is turned 180
degrees.6 Therefore, it is important to extubate the patient after the anesthesia provider has complete
access to the airway and necessary anesthesia equipment. During emergence, coughing and bucking on
the endotracheal tube should be avoided as this may cause bleeding in the surgical site, resulting in
hematoma formation.6 Extubating the patient under deep anesthesia may ameliorate this complication
7
decreasing the potential for coughing. However, the decision to extubate the patient deep versus awake
will depend on if securing the airway was easy or difficult and risk of aspiration.6,7
During this case, recognizing signs and symptoms of a hematoma was critical. Supraorbital hematoma
can quickly develop into a periorbital hematoma and a periorbital hematoma can progress into a
retrobulbar hemorrhage.8 Retrobulbar hemorrhage in turn may lead to blindness due to the untreated
pressure maintained on the optic nerve.8 Immediate assessment of the patient’s visual acuity is a priority
because changes in visual acuity can be an early indicator of retrobulbar hemorrhage.8 Additional signs
and symptoms include an afferent pupillary defect, resistance to retropulsion, proptosis or increased
intraocular pressure.8 While the consequences of a periorbital hematoma progressing to a retrobulbar
hemorrhage are detrimental, the incidence of developing a hematoma post supraorbital craniotomy is
low. A study conducted by Kabil and Shahinian (2006), looked at complications post supraorbital
endoscopic approach and indicated that there was no evidence of hematoma formation postoperatively
in their study group. Incidentally one patient in the study group developed transient swelling and
reddening of the periorbital area.
Endoscopic supraorbital craniotomy is a safe and effective method for surgically removing tumors
located at the base of the skull. Similar to other endoscopic craniotomies, this approach carries some
complications. These complications can be prevented by a meticulous surgical approach and a smooth
emergence from anesthesia. Minimal retraction and manipulation of the orbicular and frontal muscular
layer is essential to avoid a postoperative periorbital hematoma. A supraorbital hematoma can form with
greater manipulation.4 Early opioid administration, especially hydromorphone, aids in the patient’s
comfort post-extubation. This can facilitate hematoma evacuation if warranted, such as was the case
with the patient presented. Applying pressure at the surgical site during extubation may also prove
effective in prevention of hematoma formation. Supraorbital hematoma is a very rare complication that
can develop after endoscopic supraorbital craniotomy. However, as the number of patients that opt for
minimally invasive craniotomies increases, the incidence of this complication may rise.
References
1. Moon HS, Lee SK, Chung SH, Chung JH, Chang IB. Recurred pneumo pneumocephalus in a head
trauma patient following positive pressure mask ventilation during induction of anesthesia -A case
report. Korean J Anesthesiol.2010;59(suppl):S183-186.
2. Kabil MS, Shahinian HK. The endoscopic supraorbital approach to tumors of the middle cranial
base. Surg Neurol. 2006;66(4):396-401.
3. Wilson DA, Duong H, Teo C, Kelly DF. The supraorbital endoscopic approach for tumors.
[published online ahead of print February 5, 2013]. World Neurosurg. 2013;1-13.
4. Reisch R, Perneczky A. Ten-year experience with the supraorbital subfrontal approach through skin
incision. Neurosurg. 2005;57(4 Suppl):242-255.
5. Cappabianca P, Califano L., Laconetta G. Cranial, Craniofacial and Skull Base Surgery. In:
Little AS, Gore PA, Darbar A, Teo C, eds. Supraorbital Eyebrow Approach. Milan, Italy: SpringerVerlag Italia; 2010: 27 – 37.
6. Shahinian HK. Endoscopic skull base surgery: A comprehensive guide with illustrative cases. In:
Shahinian HK, eds. Anesthetic Considerations in Endoscopic Skull Base Surgery. Totowa, New
Jersey: Humana Press; 2008: 6-7.
7. Popat M, Mitchell V, Dravid R, Patel A, Swampillai C, Higgs A. Difficult Airway Society
8
Guidelines for the management of tracheal extubation. Anaesthesia. 2012:67(3):318–340.
8. Terella, AM, Wang TD, Kim MM. Complications in periorbital surgery. Facial plast surg.
2013;29(1):64-70.
Mentor: Kelly L. Wiltse Nicely, CRNA, PhD
Acute Intermittent Porphyria
Kristal Barbee, MSN
Georgetown University
Keywords: acute intermittent porphyria, ketamine, propofol, sevoflurane, sufentanil
Acute Intermittent Porphyria (AIP) is a rare, inherited disorder affecting the liver heme synthesis
pathway which is regulated by aminolevulinic acid (ALA) synthetase, the rate limiting step in
the production of heme. Many anesthetic drugs require the cytochrome P450 for metabolism,
which increases the production of ALA synthetase and thus heme. When the normal pathway is
blocked, enzyme substrates can accumulate causing an acute porphyria crisis. For patients at risk
for AIP the anesthesia provider should choose anesthetic agents that will minimize the chance of
triggering an acute porphyria attack during the peri-operative period.1-4
Case Report
A 37-year-old, 97 kg, 175 cm male, presented for a C4-C7 anterior cervical discectomy and
fusion with a diagnosis of spondylosis with myelopathy. The patient’s past medical history
included AIP with two episodes of pancreatitis requiring hospitalization within the prior six
months and report of alcohol use of undetermined frequency. The patient suffered from chronic
neck pain and was taking klonopin, gabapentin, oxycontin, and oxycodone. With the use of these
medications he reported that his level of pain was never below a 6/10. The patient had limited
neck range of motion and his airway exam indicated he was Mallampati class II.
An 18 gauge peripheral intravenous catheter (PIV) was started in the preoperative area and
midazolam 5 mg intravenous (IV) was administered before transporting him to the operating
room (OR). Upon arrival to the OR, standard monitors were placed and the patient was
preoxygenated with O2 10 L/min. The patient received lidocaine 100 mg, propofol 200 mg,
fentanyl 250 mcg, and rocuronium 50 mg IV for induction of anesthesia. The trachea was easily
intubated while using the Glidescope (Verathon Inc., Bothell, WA) with cervical spine
stabilization by a second anesthesia professional. Respirations were controlled with a mechanical
ventilator with a mixture of oxygen 1 L/min and air 1 L/min.
A second 18 G PIV, right radial arterial line, and foley catheter were placed after induction of
anesthesia. Needle electrodes were placed to monitor somatosensory evoked potentials (SSEP)
and motor evoked potentials (MEP). Anesthesia was maintained throughout the case with
sevoflurane at 0.5 minimum alveolar concentration (MAC), a propofol infusion at 100-150
mcg/kg/min for a total of 3250 mg, a sufentanil infusion of 0.3-0.5 mcg/kg/hr for a total of 230
9
mcg, which were all discontinued 30 min prior to the end of the case. He also received a 2-hour
ketamine infusion, started at the beginning of the case at 0.2 mg/kg/hr for a total of 38 mg. The
patient received dexamethasone 10 mg, cefazolin 2 g, and hydromorphone 2 mg IV prior to
incision.
Near the end of the 8-hour case, the patient received acetaminophen 1 g and ondansetron 4 mg
IV. The total IV crystalloid fluid intake was 2550 mL, blood loss was 100 mL, and 1000 mL of
clear yellow urine was recorded. At the conclusion of the case, the patient was not spontaneously
breathing or responding to noxious stimuli despite discontinuation of the sevoflurane and all
infusions. Neostigmine 5 mg with glycopyrrolate 0.6 mg was administered despite receiving only
an initial dose of rocuronium and full neuromuscular recovery as indicated by four out of four
twitches followed by sustained tetany on the neuromuscular monitor. The patient was also dosed
with naloxone 0.04 mg IV. After an hour of an unsuccessful emergence in the OR, the patient
remained intubated and was transported to the post anesthesia care unit where respirations were
controlled with a mechanical ventilator. He met criteria for extubation 1.5 hours later and was
discharged home the following day with no evidence of an acute AIP crisis.
Discussion
AIP is a rare (1:20,000), autosomal dominant inherited metabolic disease affecting the heme
synthesis pathway causing an overproduction of porphyrins.2,4,5 The synthesis of porphyrins
occurs as a result of a series of pathway enzymes. A defect, specifically in the enzyme
porphobilinogen deaminase, part of the heme synthesis pathway, is found in patients with AIP
thereby causing a buildup of pathway intermediaries, interfering with the negative feedback loop.
An increase in heme requirements, such as the induction of cytochrome P450 can result in an
accumulation of pathway intermediates. Many drugs commonly administered in anesthesia
induce ALA synthetase, which is dependent on the formation of heme. The production of ALA
synthetase is increased in order to increase production of heme in response to drugs that utilize
cytochrome P450 for drug metabolism. The increase in ALA synthetase stimulates the heme
production pathway causing an accumulation of enzymes, because of the defective
porphobilinogen deaminase and thus the production of excessive amounts of porphyrin. An acute
crisis can be caused by either a porphyrin accumulation or reduction in the production of heme.
An acute crisis is manifested as severe abdominal pain, nausea, vomiting, neuropathies,
tachycardia, or hypertension.1-4
The literature indicates that barbiturates, anti-epileptics, sulfonamide antibiotics, and ketorolac
should be avoided in patients with known AIP, whereas other medications such as opioids,
propofol, nitrous oxide, many local anesthetic agents, and neuromuscular blockers are considered
safe.1-5 Controversial medications include sevoflurane, etomidate, and ketamine which may
contribute to an acute crisis.1,3,4 It is important in the perioperative setting to be aware that other
conditions such as dehydration, alcohol use, fasting, pain, psychological stress, infection, and
nausea, and vomiting can trigger an acute attack.2,3
Propofol, opioids, rocuronium, and acetaminophen have been proven to be safe drugs and can be
administered to a patient with AIP without precipitating an acute crisis.2-5 Propofol is considered
the drug of choice for induction of anesthesia in AIP patients.2,3 Researchers and experts in
10
porphyria recommend desflurane as the preferred volatile anesthetic agent. Nitrous oxide has
also been used safely in patients with AIP.2-4,6 Enflurane is absolutely contraindicated and
evidence is inconclusive regarding the other volatile anesthetics. Although there is questionable
research pertaining to the use of sevoflurane, there have been several case reports of it safely
being used for general anesthesia,1,2,6 Ketamine is another controversial agent as the evidence is
limited and conflicting. Some experts recommend avoiding the ketamine in patients with known
AIP because they believe it can contribute to delirium that may mask an acute crisis while some
endorse its use.1,3,4 Researchers have also found that prolonged administration of any anesthetic
agent including propofol may contribute to an acute crisis; therefore, using short-acting agents
for the minimal amount of time possible is recommended.2-4
The length of the surgery, the patient’s chronic pain, and the neurosurgical monitoring required
for the surgery dictated the choice of drugs and infusions to maintain adequate anesthesia.
Additionally, his chronic pain history further complicated the choice of anesthetic agents. It was
important to maintain a satisfactory level of analgesia with a variety of drugs that act on the
various pain receptors to avoid an acute crisis.4,7
While the patient in this case did not appear to suffer an acute porphyria attack within the first
24-hours postoperatively, he had delayed emergence from anesthesia necessitating mechanical
ventilation into the recovery period. The exact cause for delayed emergence from anesthesia
could be due to a variety of factors related or unrelated to the medications given. Anecdotal case
studies and dated research guide the anesthetist’s knowledge of safe, unsafe and undetermined
safety of anesthetic drugs. In addition, the stress of surgery, infection or other factors such as
alcohol use, drugs taken by the patient prior to surgery or electrolyte disturbances may have
contributed to the delayed awakening.
Although it can never be conclusively determined the cause for the delayed awakening after
anesthesia in this case, there are factors that may have improved the outcome. Using Bispectral
Index monitoring (Aspect Medical Systems, Inc.) during this case could have better guided the
anesthetic plan. Using desflurane rather than sevoflurane may have been a better volatile
anesthetic of choice. The prolonged infusion of propofol or the combination of the several
anesthetic modalities administered may have contributed to the delayed awakening.
There is much to be discovered about AIP and the associated crises that can develop after
receiving anesthetic drugs. No current clinical research has been conducted on this rare disease
and it is unlikely that AIP will receive funding for studies. Therefore, much of the information
that is derived from anesthetic management is related to dated studies, clinical case reports, and
expert opinions available in the research. It is recommended that anesthesia professionals
continue to publish AIP case reports that discuss the specific drugs utilized in anesthesia with
their associated outcomes.
References
1. Mustajoki P, Heinonen J. General anesthesia in “inducible” porphyrias. Anesthesiology.
1980;53:15-20.
11
2. Tantawy H, Myslajek T. Inborn errors of metabolism. In Hines, RL, Marschall, KE, eds.
Stoelting’s Anesthesia and Co-Existing Disease. 6th ed. Philadelphia:Elsevier; 2012:305-310.
3. James MFM, Hift RJ. Porphyrias. Br J Anaesth. 2000;85(1):143-153.
4. Findley H, Phillips A, Cole D, Nair A. Porphyrias: Implications for anesthesia, critical
care,and pain medicine. Contin Educ Anaesth Crit Care Pain. 2012;5(15):1-6.
5. American Porphyria Foundation. http://www.porphyriafoundation.com/drug-database. 2010.
Accessed March 17, 2014.
6. Evans PR, Graham S, Kumar CM. The use of sevoflurane in acute intermittent porphyria.
Anaesth. 2001;56(4):388-389.
7. Fisher RB, Johnson QL, Reeves-Viets JL. Chronic opioid drug therapy: Implications
forperioperative anesthesia and pain management. Mo Med. 2013;110(3):231-235.
Mentor: Denise H. Tola, CRNA, MSNA
Total Intravenous Anesthesia for Malignant Hyperthermia
Michelle Marciano, MSN
Georgetown University
Keywords: malignant hyperthermia, total intravenous anesthesia, propofol infusion, laryngeal
mask airway, anesthetic triggering agents
Malignant hyperthermia (MH) is a hypermetabolic condition that occurs in genetically
susceptible patients after being exposed to an anesthesia triggering agent.1 Malignant
hyperthermia cases are rare, but can be fatal, with an estimated incidence around 1:50,000.2 The
most common triggering anesthetics include succinylcholine and all volatile anesthetic agents.1
Delivering anesthesia to a patient with a history of malignant hyperthermia presents a distinctive
anesthetic challenge. The following case explains the importance of adequate preparation and the
use of total intravenous anesthesia (TIVA) in the anesthetic management in a patient at risk for
malignant hyperthermia.
Case Report
A 29-year-old, 150 cm, 79 kg female with a left ankle fracture presented for removal of hardware
from the left ankle. Her medical history was significant for hypertension, asthma, Type 1
Diabetes, migraines, penicillin allergy, bipolar and anxiety disorders, anemia, and a personal
history of malignant hyperthermia with prior surgery. The operating room (OR) was prepared by
the anesthesia team by placing a new breathing circuit and new carbon dioxide absorbent on the
anesthesia machine. The vaporizers were removed, and the anesthesia machine was flushed with
oxygen at a rate of 10 L/min for 30 min. Different anesthesia machines and hospitals have
varying MH protocols, but all of them stress the importance of flushing the machine with
oxygen. The hospital’s standard malignant hyperthermia cart was placed inside the OR suite for
immediate access if necessary, and the contents of the cart were verified.
12
A peripheral intravenous (IV) line was started, and midazolam 2mg IV along with fentanyl 100
mcg IV was administered as premedication. A popliteal and a saphenous nerve block were
performed using 0.5% bupivacaine, and catheters were left in place for each block. Once the
patient was transported into the OR, the patient was positioned supine on the OR table, and
monitors including a pulse oximeter, electrocardiograph, noninvasive blood pressure cuff, and
cutaneous temperature probe were applied. Oxygen via face mask was administered at 12 L/min
for pre-oxygenation. The left lower extremity was assessed to be numb to touch by the surgeon.
Induction medications included lidocaine 20 mg and propofol 200 mg IV. A laryngeal mask
airway (LMA), size #4, was inserted. Bilateral breath sounds and end tidal carbon dioxide
(EtCO2) were confirmed. Oxygen via the LMA was administered at a rate of 4 L/min. A
continuous infusion of propofol was started at a rate of 100 mcg/kg/min. Vancomycin 1.5 g IV
was administered as antibiotic therapy.
The patient maintained spontaneous ventilation through the LMA, with EtCO2 between 35 and
40 mm Hg. The patient remained hemodynamically stable, with a heart rate between 60 and
75/min and systolic blood pressure ranging from 110 to 140 mm Hg. Titration of the rate of the
propofol infusion and fentanyl boluses was based on patient movement and vital signs, such as
tachycardia or hypertension.
In total the patient received propofol 800 mg and fentanyl 450 mcg throughout the entire 120min case. The patient received 1200 mL of Lactated Ringers and estimated blood loss was 15
mL. Ondansetron 4 mg IV was administered as an antiemetic. The patient was transferred to the
Post Anesthesia Care Unit (PACU) where she remained for an additional 120 min. She required
fentanyl 50 mcg IV bolus three times for pain scores of 6 out of 10, for a total of fentanyl 150
mcg. In addition, the block team re-dosed her popliteal and saphenous nerve blocks with diluted
bupivacaine for postoperative pain relief via block catheters. Vital signs remained at baseline. No
tachycardia, sweating, hyperthermia, arrhythmias, muscle rigidity, or change in urine color noted
throughout the procedure.
Discussion
Malignant hyperthermia is a hypermatabolic condition generally occurring in genetically
susceptible patients, typically with an autosomal dominant mutation, after being exposed to
an anesthetic triggering agent.1 The triggering anesthetics include all inhalational agents and
succinylcholine, a depolarizing neuromuscular blocker.2 Malignant hyperthermia is most likely
caused by a reduction in the reuptake of calcium by the sarcoplasmic reticulum, which is needed
to stop muscle contraction. When this occurs, muscle contraction is sustained, causing signs of
hypermetabolism and hyperthermia.1,3
A personal or family history of anesthetic problems, such as unexplained fevers or death during
anesthesia, or personal history of malignant hyperthermia suggests susceptibility for malignant
hyperthermia, and the anesthesia plan should take special attention to avoid a crisis.1 The MH
cart, with 36 vials of dantrolene, should be available in the OR should a crisis occur. Dantrolene,
a muscle relaxant, is the treatment for MH, inhibiting calcium release from the sarcoplasmic
reticulum.3 Due to the possibility of residual inhalational agent, the anesthesia machine needs to
be prepared by changing the carbon dioxide absorbent and fresh gas tubing, disconnecting the
13
vaporizers, using a disposable breathing circuit, and flushing the machine with oxygen at a rate
of 10 L/min for at least 10 minutes.1,2 My hospital policy suggests flushing the machine for 30
minutes, so that is what we did. Local or regional anesthesia should be considered, but general
anesthesia using non-triggering agents is acceptable.1 In this case, peripheral nerve blocks were
administered preoperatively, however it was determined that the blocks were not going to
provide adequate pain relief alone, and TIVA was needed for general anesthesia.
Larach et al studied 291 cases involving patients that experienced a malignant hyperthermia
event, and reported that 8 (2.7%) resulted in cardiac arrests and 4 (1.4%) resulted in death.4 Early
signs of malignant hyperthermia should be closely monitored, so treatment can be initiated
immediately. Early clinical signs include elevated CO2, sweating, tachycardia, arrhythmias,
unstable arterial pressure, masseter spasm, and muscle rigidity. Later signs include
hyperkalemia, hyperthermia, elevated blood creatine phosphokinase and blood myoglobin levels,
dark colored urine associated with myoglobinuria, and cardiac arrest.2 If MH is suspected,
discontinue all triggering agents, hyperventilate with 100% oxygen at high flow, convert to
TIVA if not already using this method, stop surgery, disconnect the vaporizer, change the circuit
and machine, obtain labs, and treat symptoms appropriately.1,2 Dantrolene 2.5 mg/kg IV (to
maximum dose of 10 mg/kg) should be administered. Larach et al also reported that the mortality
rate for MH was 70% without Dantrolene administration, but decreased to 1.4% when promptly
treated with Dantrolene.4
Inhalational agents had to be avoided in this patient because of her personal history of MH, so
general anesthesia was maintained with a propofol infusion and fentanyl boluses. Propofol is
considered the most suitable anesthetic agent for TIVA.5 Propofol allows for quick changes in
anesthetic depth, and a speedy recovery, due to its ability to be rapidly metabolized. The low
context–sensitive halftime makes propofol the best available agent for TIVA procedures.3,5
Lastly, propofol attenuates airway reflexes so the LMA may be positioned easily without
neuromuscular blockade, which was useful in this case.5
Since the patient was a low risk for aspiration, surgical time was under 2 hours, and
succinylcholine had to be avoided, an LMA was used to maintain the patient’s airway during the
case as opposed to an endotracheal tube (ETT). Researchers at the University of Cape Town
found that the LMA, compared to the ETT, was a safe alternative airway during TIVA. This
study compared four groups of patients receiving TIVA with either an LMA or an ETT, and
either neuromuscular blockade or no blockade. The study found that the patients in the group
with an LMA and no neuromuscular blockade were more hemodynamically stable than those
with an ETT. The LMA was found to be an effective device during TIVA, and easier to manage
than the ETT in the absence of neuromuscular blockade.6 Since neuromuscular blockade was not
utilized in this case, the LMA was a safe alternative airway.
As an anesthesia practitioner, avoiding MH in a susceptible patient, while maintaining general
anesthesia and a hemodynamically stable patient, was my goal. Recognizing this patient was at
high risk for MH because of her personal history of MH, an anesthetic without any triggering
agents was necessary. TIVA with a propofol infusion and fentanyl boluses, along with both a
popliteal and saphenous nerve block, was my choice to diminish the risk of anesthetic
complication, since it avoided inhalational anesthetics and succinylcholine. The patient’s post
14
anesthesia course, both without excruciating pain or any signs of MH, confirmed the anesthetic
was a success. In future cases, TIVA could be established with dexmedetomidine instead of
propofol, since new studies are showing how this alpha-2 agonist provides safe and effective
sedation, amnesia, and analgesia without respiratory depressant effects, and without triggering
MH.
References
1. Bloom J, Baker K. Intra-anesthetic problems. In Levine W, ed. Clinical Anesthesia
Procedures of the Massachusetts General Hospital. 8th ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2010:285-287.
2. Glahn K, Ellis F, Halsall P, et al. Recognizing and managing a malignant hyperthermia crisis:
guidelines from the european malignant hyperthermia group. British Journal of Anesthesia.
2010;105(4):417-420.
3. Wouden J, Miller K. General anesthetic pharmacology. In Golan D, ed. Principles of
Pharmacology the Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2007:240-264.
4. Larach M, Brandom B, Allen G, Gronert G, Lehman E. Cardiac arrests and deaths associated
with malignant hyperthermia in north america from 1987 to 2006: a report from the north
american malignant hyperthermia registry of the malignant hyperthermia association of the
united states. Anesthesiology. 2008;108(4):603-611.
5. Salih A. The laryngeal mask airway: technical guidelines and use in special situations. The
Iraqi Postgraduate Medical Journal. 2006;5(2):230-239.
6. Dyer R, Llewellyn R, James M. Total i.v. anesthesia with propofol and the laryngeal mask
for orthopaedic surgery. Br J Anaesth. 1995;74:123-128.
Mentor: Catherine Horvath, CRNA, MSN
High Spinal in a Morbidly Obese Patient
Verity Caruso, MS
Westminster College
Keywords: high-spinal, total spinal, morbid obesity, spinal anesthesia, neuraxial anesthesia
High and total spinals are acute, potentially life threatening risks of spinal anesthesia, occurring
when the cephalad spread of the local anesthetic (LA) results in an unexpected high
neuroblockade.1 The morbidly obese are a rapidly growing segment of the United States
population.2-4 There is evidence that increased BMI correlates to increased block height with
neuraxial anesthesia.2 This suggests that the morbidly obese may be at increased risk of high or
total spinals when dosing is not adjusted in this population.. Symptoms of high and total spinals
must be identified and treated early, to prevent devastating consequences, even death.1
15
Case Report
A 170 cm, 141 kg, 64-year-old male with a BMI of 48.7 kg/m2 was scheduled for a total knee
arthroplasty due to osteoarthritis. His medical history included: morbid obesity, osteoarthritis,
hypertension, atrial fibrillation, obstructive sleep apnea (OSA), and diabetes mellitus. The
patient’s current medications included: warfarin, potassium chloride, furosemide, lisinopril,
testosterone, bupropion, diltiazem, metformin and simvastatin. He had no known drug allergies.
The last dose of warfarin was five days preceding surgery and the international normalized ratio
was 1.2.
In the preoperative area intravenous access was secured, oxygen was administered by nasal
cannula at 4 L/min, noninvasive monitors were applied, and midazolam 4 mg was given before
peripheral nerve blocks were placed. Femoral and sciatic blocks were achieved each using 20
mL ropivacaine 0.5%. A catheter was threaded into the femoral nerve block space and secured.
Replacement of the patient’s calculated fluid deficit was started preoperatively as spinal
anesthesia was planned for the surgery. One liter of Lactated Ringer’s (LR) solution had been
infused before the patient was taken to the operating room.
In the operating room, oxygen administration was continued by nasal cannula and noninvasive
monitors were reapplied. The patient was placed in the sitting position to perform the
subarachnoid block (SAB). Due to the patient’s body habitus we were unable to locate bony
landmarks indicative of the lower lumbar interspaces nor determine exactly which interspace was
injected. The injection site was the lowest level where spinous processes were palpable. Visually,
the space injected was estimated to be approximately L1. Free flow of cerebrospinal fluid was
confirmed via aspiration. No blood was aspirated and the patient experienced no paresthesias
during placement of the SAB. Isobaric 0.5%bupivacaine 3 mL was injected at a moderate speed
through a 22 gauge Whitacre needle.
Immediately after SAB placement the patient was assisted to the supine position. Shortly after
lying supine, he became nauseated and pale and complained of difficulty breathing. His blood
pressure decreased from 166/83 mm Hg to 96/38 mm Hg and his heart rate decreased from 78 to
53/min. The patient’s voice deteriorated into a whisper and he was minimally able to lift his
upper extremities off the bed. A high spinal was recognized. Rapid infusion of one liter of LR
solution and two phenylephrine doses of 100 mcg each were administered. His heart rate
remained in the mid-50s with administration of phenylephrine.
Preoxygenation was achieved by face mask through the anesthesia circuit at 10 L/min; mask
ventilation was easy with placement of an oral airway. Rapid sequence induction with propofol
140 mg and succinylcholine 200 mg was used to facilitate tracheal intubation for mechanical
ventilation. Anesthesia for tolerance of the endotracheal tube was maintained with sevoflurane
1.0% expired concentration and oxygen at 2 L/min. A phenylephrine infusion was required
intermittently throughout the surgery to maintain a mean arterial blood pressure greater than 65
mm Hg.
At the end the surgical case (3 hours), the patient was spontaneously ventilating. Emergence
from general anesthesia and extubation of the trachea were uneventful. The patient was
16
transferred to the recovery area with oxygen by non-rebreather facemask. Recovery and
postoperative period were uneventful and patient was discharged without sequelae.
Discussion
Morbid obesity, a BMI of 40 or more,2-5 affected 15.5 million Americans by 2010.4 Trend
estimates suggest the rate of morbid obesity continues to rise rapidly.4 Numerous health
problems associated with morbid obesity cause this population to require or desire surgery
frequently.2,3
Regional anesthesia presents several advantages and challenges for the morbidly obese.2,3
Potential advantages include: minimal airway manipulation, less cardiopulmonary depression,
better postoperative pain control with decreased use of opioids, reduced postoperative nausea
and vomiting, shorter lengths of stay in both post-anesthesia care units and hospitals, fewer
complications, and fewer unplanned hospital admissions.2 Challenges include: positioning,
difficulty identifying landmarks, fat pockets resulting in false-positive loss of resistance during
needle placement, needing longer needles, increased incidence of accidental dural puncture or
epidural venous puncture, and ineffective blocks more often than in the nonobese population.2,3,5
Despite technical challenges of placing a SAB and conflicting data regarding local anesthetic
dosing, the actual incidence of complications seems to be low in obese patients.2 This patient’s
history of morbid obesity and OSA made SAB an appropriate choice for his anesthesia.
Two significant, potential complications of SAB are high and total spinals.6 A high spinal affects
vasomotor tone, and therefore blood pressure, when LA spread blocks the sympathetic fibers
arising from T5-L1.6 When LA reaches the T1-T4 (cardiac accelerator fibers), heart rate is
affected (bradycardia).6 A total spinal occurs when the local anesthetic affects the entire spinal
cord and possibly the brainstem.1 Respiratory depression and unconsciousness accompany
hypotension and bradycardia in a total spinal.5
If a high or total spinal occurs, prompt recognition and intervention are key to preventing
permanent damage or death.1 The first symptoms that LA has reached a higher level than
intended are often dyspnea, and numbness, tingling, or weakness in the upper extremities.6
Nausea commonly precedes hypotension. As cervical spinal nerves are affected, patients exhibit
severe hypotension, bradycardia, difficulty speaking and respiratory insufficiency. A total spinal
results in loss of consciousness and apnea. If unrecognized and untreated, hypotension,
bradycardia and hypoxemia lead to cardiac arrest. However, outcomes are improved when
respiratory and cardiovascular system depression are quickly identified and supported.1,6 In this
case, the patient’s BP was supported with vasopressors and fluid and his respiratory system
supported by intubation of his trachea and mechanical ventilation. Interventions were swift and
the patient suffered no long term effects.
Many factors may contribute to increased cephalad spread of LAs in the intrathecal space.1,6
Such factors include: dose-related factors of volume, dosage, and baricity; administration
technique including needle type, site of injection, needle direction, injection velocity and use of
17
barbotage; and patient characteristics such as height, age, gender, intra-abdominal pressure and
anatomy of the spinal cord.1,6
Morbid obesity alters drug distribution,2,5 but there is conflicting data as to whether obesity
affects the spread of local anesthetics in neuraxial anesthesia.5 Some studies have found lower
anesthetic requirements for neuraxial anesthesia in obese patients when compared to non-obese
patients3,5 or a strong correlation between increasing BMI and sensory block height.2 Yet other
studies demonstrated no correlation between BMI and the spread of local anesthetic in neuraxial
anesthesia.2,5 There is a paucity of information regarding how morbid obesity affects regional
anesthesia, thus controversy remains as to whether smaller local anesthetic doses should be used
for neuraxial anesthesia in obese patients.2
When landmarks are impalpable, lumbar ultrasonography has been used to aid neuraxial
placement in obese patients.2,5,7 Imaging can determine the correct interspinous space, accurately
identify midline and estimate depth of the ligamentum flavum and dura in most patients.7 In
cases of extreme obesity, ultrasound guidance may only aid in identifying spinous processes and
midline.5 Many of our patient’s bony landmarks could not be palpated, making him an
appropriate candidate for ultrasound guidance. Experience in US use and required equipment is
paramount in applying this technology.
Anesthetic management of the morbidly obese is challenging. Because the prevalence is
increasing rapidly, we must identify ways to safely and effectively provide anesthesia for this
population. Though regional anesthesia is commonly a safe mode in this population, placement
of blocks can often be technically difficult. Ultrasound guidance for placement of neuraxial
blocks is one way to mitigate the challenge. Furthermore, continued research is needed to
determine dosing guidelines and techniques for this population.
References
1. Bernards CM. Epidural and spinal anesthesia. In: Barash PG, Cullen BF, Stoelting RK,
Cahalan MK, Stock MC, eds. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2009:927-954
2. Brodsky JB, Mariano ER. Regional anaesthesia in the obese patient: lost landmarks and
evolving ultrasound guidance. Best Pract Res Clin Anaesthesiol. 2011;25(1):61-72.
doi:10.1016/j.bpa.2010.12.005.
3. Ingrande J, Brodsky JB, Lemmens HJ. Regional anesthesia and obesity. Curr Opin
Anaesthesiol. 2009;22(5):683-686. doi:10.1097/ACO.0b013e32832eb7bd.
4. Sturm R, Hattori A. Morbid obesity rates continue to rise rapidly in the United States. Int J
Obes (Lond). 2013;37(6):889-891. doi:10.1038/ijo.2012.159.
5. Whitty RJ, Maxwell CV, Carvalho JC. Complications of neuraxial anesthesia in an extreme
morbidly obese patient for Cesarean section. Int J Obstet Anesth. 2007;16(2):139-144.
doi:10.1016/j.ijoa.2006.08.011.
6. Kleinman W, Mikhail M. Spinal, epidural, and caudal blocks. In: Morgan GE, Mikhail MS,
Murray MJ, eds. Clinical Anesthesiology. 4th ed. New York, NY: Lange Medical
Books/McGraw-Hill Companies; 2006:289-323.
18
7. O’Donnell D, Prasad A, Perlas A. Ultrasound-assisted spinal anesthesia in obese patients. Can
J Anesth. 2009;56(12):982-983. doi:10.1007/s12630-009-9179-6.
Mentor: Manardie Shimata, CRNA, MAE
Acknowledgement: Wynn Sperry, CRNA
Anesthetic Management of a Patient with Myasthenia Gravis
Camille Y. Higdon, BA, BSN
Wake Forest Baptist Health
Keywords: Myasthenia Gravis, Autoimmune Neuromuscular Disorder, Neuromuscular Junction,
Acetylcholine Receptors
Myasthenia Gravis (MG) is an autoimmune neuromuscular disorder affecting predominantly
young women and older men, the prevalence in the United States is estimated at 0.5-14.2 per
100,000.1 The hallmark of this disease is the destruction of nicotinic receptors resulting in
reduced synaptic transmission at the neuromuscular junction leading to incomplete or absent
muscle depolarization. Symptoms include skeletal muscle weakness exacerbated by activity and
relieved by rest. Individuals affected by MG have an unpredictable response to illness, stress and
pregnancy and can exhibit a range of symptoms involving weakness of the ocular muscles to
respiratory failure described as myasthenic crisis.2
Case Report
A 63 year-old, 62 kg, 160 cm tall female patient with a past medical history significant for MG
but otherwise healthy experiencing pain and numbness in her lower back and bilateral upper legs
presented for a minimally invasive lumbar discectomy of L3-L4. The patient takes
pyridostigmine 60 mg daily and noted an increased prednisone dose to 7 mg daily to control
symptoms over the previous 12 months. An 18 gauge intravenous catheter was obtained in the
left hand and a lactated ringers infusion was initiated. The patient was premedicated with
fentanyl 50 mcg prior to transport to the operating room.
Upon arrival in the operating room, noninvasive monitoring was initiated and preoxygenation
was provided with oxygen 10 L/min. General anesthesia was induced with lidocaine 50 mg,
propofol 140 mg and alfentanil 1000 mcg. Laryngoscopy was performed with a Mac 3 blade and
the trachea was intubated with a 6.5 mm cuffed oral endotracheal tube. Placement was confirmed
with bilateral breath sounds and end tidal CO2. Intraoperatively respirations were controlled with
volume controlled mechanical ventilation and a fresh gas flow totaling 2 L/min of an equal
mixture of oxygen and air. General anesthesia was maintained with a continuous infusion of
remifentanil titrated between 0.15-0.2 mcg/kg/min and isoflurane 1%. The patient’s eyes were
lubricated and taped prior to prone positioning on the operating table for optimal surgical
exposure. Pressure points were padded, arms were abducted less than 90 degrees, eyes and ears
were free from pressure. Prophylactic antibiotics were administered as well as supplemental
corticosteroids, cefazolin 1 g and dexamethasone 10 mg respectively.
19
Approximately 30 minutes prior to the end of the case, ondansetron 4 mg was administered and
the isoflurane was discontinued and general anesthesia was maintained with fresh gas mixture of
N2O 2 L/min, O2 1 L/min and remifentanil 0.2 mcg/kg/min. After the closing sutures were
completed by the surgeon, the patient was turned supine onto the stretcher, all agents were
discontinued and oxygen flow was increased to 10 L/min. As the patient began to initiate
spontaneous respirations, mechanical ventilation was discontinued and manual positive pressure
ventilation was initiated. Once adequate tidal volumes were reached at a rate within normal
limits and the patient opened her eyes to command she was extubated and transported with
supplemental oxygen 10 L/min via face mask to the post anesthesia care unit. Muscle weakness
was assessed according to bilateral strength of hand squeeze and dorsiflexion of the feet. The
patient exhibited no signs of weakness with these actions. The patient’s postoperative recovery
was uneventful without respiratory complications and the patient was discharged home the same
day.
Discussion
Myasthenia Gravis is a chronic autoimmune neuromuscular disorder in which the nicotinic
acetylcholine receptors at the motor end-plate of skeletal muscles are inactivated by circulating
autoantibodies and complement mediated destruction. The weakness associated with the disease
manifests in different patterns ranging from involvement of only specific muscle groups such as
ocular muscles to generalized fatigability affecting the bulbar and limb muscles. Patients with
MG may present with symptoms of laryngeal and pharyngeal muscle weakness resulting in
dysphagia, dysphonia and difficulty clearing secretions leading to an increased risk for
aspiration. A more severe manifestation of the disease includes respiratory muscle weakness
resulting from illness, infection, emotional stress, or surgery which can lead to respiratory failure
described in the literature as Myasthenic crisis.3
The hallmark treatment of MG patients are cholinesterase inhibitors such as pyridostigmine
which flood the neuromuscular junction with acetylcholine increasing the availability of
acetylcholine for activation of intact nicotinic receptors. Pyridostigmine should be continued in
the perioperative period.5 However, when anticholinesterase agents are used perioperatively
patients taking pyridostigmine are at risk for cholinergic crisis resulting from overstimulation of
muscarinic receptors leading to symptoms of salivation, lacrimation, urination, defecation, GI
distress and emesis (SLUDGE).1
As the disease increases in severity, corticosteroids and immunomodulators are often included in
the pharmacological management of the disease. This patient’s history of chronic corticosteroid
therapy as part of her treatment regimen and noted increase in prednisone consumption over the
previous twelve months prior to her surgery indicated that a stress dose of supplemental
corticosteroids be administered intraoperatively.2
Patients with MG are often sensitive to the respiratory depressant effects of narcotics and
benzodiazepines and should be used with caution preoperatively.3 For this reason midazolam
was not included in the anesthetic plan, however, a low dose of fentanyl was safely administered
prior to transport to the operating room in order to relieve pain and anxiety verbalized by the
patient.
20
Myasthenia Gravis patients often exhibit a profoundly increased sensitivity to non-depolarizing
neuromuscular relaxants (NDMRs) due to the decreased number of functional acetylcholine
receptors and may lead to prolonged intubation and/or residual muscle weakness
postoperatively.2 As a result, NDMRs should only be included in the anesthetic plan for these
patients when absolutely necessary, given at decreased doses and with close attention to
neuromuscular monitoring.3 The response to depolarizing agents is often unpredictable. Patients
can exhibit a resistance to succinylcholine or to the anticholinesterase medications with which
these patients are medically managed, and may lead to a prolonged duration of action.2 These
medications were excluded from the anesthetic plan in order to avoid potential complications of
increased sensitivity and prolonged time to extubation. Alternatively, short acting opioids were
chosen for induction and maintenance of anesthesia for this case based on the observation that
the muscle weakness associated with MG often allows for tracheal intubation. Additionally,
volatile anesthetics have neuromuscular blocking properties which are often magnified in MG
patients with the added benefit of no residual block after these agents are discontinued.3
For this patient, tracheal intubation was accomplished using propofol, isoflurane and alfentanil.
Alfentanil has been shown to provide optimal intubating conditions when NDMRs are
contraindicated.4 Respiratory depression results from alfentanil rapidly crossing the blood brain
barrier with an equilibration time significantly lower than that of fentanyl and sufentanil and was
chosen based on the rapid pharmacokinetics of onset and elimination of the drug. Maintenance of
anesthesia relied on isoflurane and remifentanil to provide adequate amnesia, analgesia and
akinesia. Remifentanil was used in consideration of the respiratory effects of longer acting
opioids. These agents can persist into the postoperative period and the desire was for this patient
to exhibit a strong respiratory drive at extubation and in recovery. The drug was chosen owing to
metabolism by non specific blood and tissue esterases which allows for rapid clearance.4
Additionally, remifentanil has also been shown to enhance the volatile anesthetic properties that
produce akinesia and therefore provided an excellent adjuvant in this case.
Respiratory muscle weakness and respiratory depression are key concerns in caring for a patient
with MG and should be closely monitored for ensuring that the patient exhibits adequate strength
to maintain spontaneous respirations postoperatively. Though all muscle relaxants were avoided
in this case, it remains important to establish that the opioid infusion has adequately metabolized
to the point that respirations are no longer inhibited. For this patient, after the remifentanil
infusion was discontinued adequate respiratory drive and rate with sufficient tidal volumes was
ensured to confirm the safety of extubation. The patient’s strength was also evaluated with hand
squeezes and plantar/dorsiflexion which was strong and equal bilaterally. The patient was able to
follow commands and showed no signs of weakness during emergence and throughout the
recovery period.
Planning an anesthetic for a patient with MG can be challenging due to the increased sensitivity
of these patients to anesthetic medications as well as the risk for disease exacerbation that can
result from surgical stress. It is important to consider the potential complications that can
accompany the inclusion of muscle relaxants in the anesthetic plan for patients with Myasthenia
Gravis.
21
References
1. Jamal BT, Herb K. Perioperative management of patients with myasthenia gravis:
Prevention, recognition and treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2009;107:612-615.
2. Butterworth IV JF, Mackey DC, Wasnick JD. Anesthesia for patients with neuromuscular
disease. In: Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan & Mikhail's Clinical
Anesthesiology. 5th ed. New York: McGraw-Hill; 2013:747-758.
3. Blichfeldt-Lauridsen L, Hansen, BD. Anesthesia and Myasthenia Gravis. Acta Anasethesiol
Scand. 2012;56:17-22.
4. Imani F, Alebouyeh MR, Taghipour-Anvari Z, Faiz SHR. Use of remifentanil and alfentanil
in endotracheal intubation: A comparative study. Anesth Pain. 2011;1(2):61-5.
5. Turakhia P, Barrick B, Berman J. Patients with neuromuscular disorder. Med Clin North Am.
2013;97:1015-1032
Mentor: Barbara Brown, CRNA, MSN
Bradycardia during Robotic-Assisted Cystoprostatectomy
Carolyn C. Hartle, BSN
Wake Forest Baptist Health
Keywords: hemodynamic changes robotic, cystoprostatectomy, robotic-assisted prostatectomy,
bradycardia with insufflation, abdominal insufflation risks
A robotic-assisted cystoprostatectomy is a minimally invasive surgery which allows the surgeon
to perform the procedure by remotely controlling surgical instruments attached to robotic arms.1
Major advantages to robotic-assisted procedures include surgical precision, decreased blood loss,
decreased post-surgical pain, faster recovery, smaller incisions, decreased risk of infections,
minimal scarring, and shorter hospital stays.2 However, they require lengthy positioning of the
patient in a steep Trendelenburg position (30°-45°), and also involve insufflation of carbon
dioxide (CO2) into the peritoneal cavity, producing pneumoperitoneum. The pneumoperitoneum
and alteration of position elicit changes in the patient’s cardiovascular system, altering the
patient’s hemodynamics.2
Case Report
A 69-year-old, 188 cm, 90 kg male with a history of bladder cancer presented for a robot-assisted
cystoprostatectomy with conduit diversion, a pelvic lymph node dissection, and an open bilateral
ureteral stent placement. He also had a history of poorly controlled insulin dependent diabetes
mellitus, chronic obstructive pulmonary disease, carotid artery disease, and cystoscopy with
transurethral resection of a bladder tumor one month prior to the current surgery. His medication
regime included gabapentin, glyburide-metformin, lorvastatin, albuterol, and insulin detemir.
The pre-anesthetic evaluation was completed in the pre-anesthesia clinic, where the patient’s preexisting conditions were optimized for surgery. The risks related to anesthesia were discussed
with the patient before the anesthesia consent was signed.
22
Midazolam 2 mg and fentanyl 100 mcg were given intravenously (IV) in the holding room. In
the operating room, standard non-invasive monitors were applied. The patient was
hemodynamically stable with a heart rate of 62/min. The patient was pre-oxygenated and was
given fentanyl 50 mcg, lidocaine 100 mg, propofol 150 mg, and rocuronium 50 mg for induction
of general anesthesia. Successful tracheal intubation with a 7.5 mm endotracheal tube was
verified and the endotracheal tube was secured.
Anesthesia was maintained with an inspired isoflurane concentration of 1%. The patient was
secured on the bed with his arms padded and tucked. The bed was moved into a steep
Trendelenburg position as a trial for hemodynamic and ventilatory stability during surgery. The
patient’s vital signs, tidal volumes, and peak inspiratory pressures remained stable during this
trial. The patient was then positioned in low lithotomy position, and the surgical team began
preparation of the abdomen for surgery. The abdomen was insufflated with CO2 by the surgeon.
During insufflation the patient’s heart rate decreased from 62 to 30 beats per minute. Ephedrine,
20 mg was given IV, with no immediate response. Glycopyrrolate 0.2 mg IV was then given.
The patient’s heart rate increased to 60/min and remained stable at that level for the remainder of
the case. There was no interruption of abdominal insufflation. The rest of the anesthetic course
was uncomplicated.
Once the robotic portion of the procedure was completed, the patient was placed into the supine
position for the remainder of the surgery. At the conclusion of surgery, neuromuscular blockade
was antagonized with neostigmine 3 mg and glycopyrrolate 0.4 mg. When the patient resumed
spontaneous respirations and appropriately followed commands, the trachea was extubated.
Oxygen at 6 L/m was administered via a Mapleson C circuit. The patient was transferred to the
post-operative care unit in stable condition.
Discussion
In the past decade, robotic-assisted cystectomy and prostatectomy surgeries have become more
common due to reports of shorter recovery periods, shorter hospital stays, and earlier return to
daily activities compared with open radical cystectomy and prostatectomy surgeries.3 However,
some studies have shown significant hemodynamic changes during robot-assisted laparoscopic
prostatectomies and cystectomies when patients were in the steep Trendelenburg position (30°45°) with high-pressure CO2 pneumoperitoneum.3,4 Several of these patients had no significant
cardiac history.4-6 Of these reported cases, the patients’ heart rate returned to baseline after
removal of the CO2.4
It is well known that using CO2 for pneumoperitoneum has risks of cardiovascular changes, such
as bradycardia and cardiac arrest. During CO2 insufflation, traction and pressure is exerted onto
the mesentery. Rapid peritoneal distention with abdominal insufflation causes a vagal-mediated
cardiovascular reflex. This reflex occurs from both decreased venous return to the heart and
stimulation of the celiac plexus in the abdominal cavity.5,7 The pressure on the mesentery from
the pneumoperitoneum stimulates the vagus nerve which decreases the patient's heart rate.7 The
bradycardia could also be a paradoxical reflex-induced response resulting from decreased venous
return. This response activates the vagal response through baroreceptors and stretch receptors.7
23
There are several treatment options when this reflex is stimulated. Pharmacological
interventions, like in the above case, are simple, effective methods to increase the patient’s heart
rate. Treating bradycardia with medication prevents interruption in the surgery and causes
minimal to no harm to the patient. The risks associated with pharmacologic treatment include a
failed desired response and a prolonged episode of bradycardia. This delay could decrease the
patient’s cardiac output, decrease perfusion to primary organs, and possibly result in asystole.
However, the anesthesia provider and the surgeon could minimize the pathophysiologic changes
from the pneumoperitoneum by limiting the intra-abdominal pressure below 12-15 mm Hg. This
can also be accomplished by keeping the rate of insufflation slow instead rapid. By decreasing
stimulation to the celiac plexus, the patient’s heart rate should return to baseline.
Several studies have demonstrated the effectiveness of these techniques. In one study, a patient
became asystolic and was treated immediately by decreasing the insufflation pressure on the
abdomen. The patient was also given chest compressions and pharmacological intervention,
which resulted in a return of spontaneous circulation.5 Other patients studied were only treated
with pharmacological intervention and had positive results, such as the patient in the case report.5
However, it is unclear in this study what pharmacological drugs were given.
When the reported patient started to show signs of bradycardia during insufflation, ephedrine
was given to stimulate beta-1 receptors and increase the heart rate. When a response to the
ephedrine was not seen, glycopyrrolate was given to block muscarinic receptors, which should
also result in an increased heart rate. Within 1 to 2 minutes of giving the glycopyrrolate and 4
minutes of giving the ephedrine, the patient’s heart rate returned to baseline. Additionally, the
surgeon could cease abdominal insufflation or decrease the intra-abdominal pressure. If the
previous interventions were unsuccessful in stabilizing the patient’s heart rate, the patient’s
position could be changed from steep Trendelenburg to flat supine. By deflating the insufflation
pressure and positioning the patient supine, venous return would increase and the vagal reflex
would be inhibited.7
In the present case, the patient’s bradycardia was treated with pharmacological interventions
prior to changes in abdominal insufflation pressure or positional changes. The patient’s positive
response from the pharmacological intervention prevented any delay in the surgery. After
treatment, the patient’s baseline heart rate was maintained. The perioperative management of
robotic-assisted urologic surgeries creates both advantages and challenges, but the literature on
hemodynamic changes during these surgeries is limited. Several studies observed physiological
effects of pneumoperitoneum in the Trendelenburg position; however, only one study discusses
successful treatment for these adverse events.5,6,8
In conclusion, the perioperative management of a patient during robotic-assisted prostatectomy
or cystectomy can bring challenges that both the surgeon and the anesthesia provider must
anticipate. Close coordination between the anesthesia and surgical teams is required for a
successful surgery.8 This case presents the anesthetic management of a patient with
complications consistent with existing current literature and best available evidence. However,
further research is needed to examine management techniques that benefit patients who have
unexpected hemodynamic changes during robotic-assisted urologic surgeries.
24
References
1. Johnson D, Castle E, Pruthi R, et al. Robotic intracoporeal urinary diversion: ileal conduit. J
Endourology. 2012;26(12):1566-1569.
2. Estey, EP. Robotic prostatectomy: The new standard of care or a marketing success?
Canadian Urological Association Journal. 2009;3(6):488–490.
3. Sung H, Ahn, J, Seo S et al. Open and Robot-Assisted Radical Cystectomy. Journal of
Endourology. 2012;26(6):670-675
4. Darlong V, Kunhabdulla N, Pandey R, et al. Hemodynamic changes during robotic radical
prostatectomy. J Anaesth. 2012;6(3):213-218
5. Gainsburg D, Wax D, Reich D, Carlucci J, et al. Intraoperative Management of RoboticAssisted Versus Open Radical Prostatectomy. Journal of the Society of Laparoendoscopic
Surgeons. 2010;14(1):1–5
6. Reed D, Nourse P. Persistent occurrence of bradycardia during laparoscopic
cholecystectomies in low-risk patients. Journal of Laparoendoscopic & Advanced Surgical
Techniques. 2009;8(2):109-114.
7. Watson, K. Abnormalities of Cardiac Conduction and Cardiac Rhythm. In Hines RL,
Marschall KE, eds. Stoelting’s Anesthesia and Co-Existing Disease. 6th ed. Philadelphia:
Churchill Livingstone; 2008:92
8. Danic MJ, Chow C, Alexander G, et al. Anesthesia considerations for robotic-assisted
laparoscopic prostatectomy: a review of 1,500 cases. J Robotic Surg. 2007;1(2):119–123.
Mentor: Phyllis McCutchen, CRNA, MSN
Preoperative ACE inhibitor use and Refractory Hypotension
Stephanie L. Anderson, BSN
Wake Forest Baptist Health
Keywords: angiotensin-converting enzyme inhibitor (ACEI), perioperative hypotension,
refractory hypotension, vasopressin, anesthesia
Over 60 million Americans are diagnosed with hypertension and currently receiving treatment.
Several classes of drugs are used to effectively control hypertension.1 Angiotensin-converting
enzyme inhibitors (ACEI) are frequently used for their additional therapeutic effects including;
stabilization of atherosclerotic plaques, inhibition of left ventricular hypertrophy, prevention of
myocardial remodeling, decreased systemic vascular resistance, decreased platelet aggregation,
decreased intraglomerular pressure, decreased fluid retention, increased insulin sensitivity and
anti-inflammatory properties.1 While these effects are important when used preoperatively, a
review including 434 patients revealed 100% use of vasopressors for intraoperative hypotension
associated with ACEI use prior to surgery. 2 This hypotension proves an intraoperative challenge
when refractory to standard treatment by anesthesia professionals.
Case Report
A 66-year-old African American female (83 kg, 160 cm) presented for a deep inferior epigastric
perforator (DIEP) flap, related to history of breast cancer and mastectomy. The patient had no
25
known drug allergies, no history of smoking or alcohol use. Additional medical history included
hypertension, hyperlipidemia, fatty liver, lymphedema of her right arm and anemia. Her
medications included metoprolol, lovastatin, acetylsalicylic acid, letrozole, chlorthalidone, multivitamin, and venlafaxine. Surgical history included: hysterectomy, nasal endoscopy,
dacryocystorhinoplasty and mastectomy. She reported no anesthetic complications following
these procedures.
She presented to the pre-operative clinic 13 days before scheduled surgery with a blood pressure
(BP) of 188/98 mm Hg and a mean arterial pressure (MAP) of 128 mm Hg, and was referred to
her primary care provider for improved control of hypertension prior to surgery. She was
prescribed lisinopril, she self-administered metoprolol and lisinopril the morning of surgery. The
morning of surgery her BPe was 178/89 mm Hg (MAP 118 mm Hg). A complete pre-anesthetic
evaluation revealed no other significant findings. Lab values were within normal limits. Physical
examination revealed a Mallampati Class III, thyromental distance of three fingerbreadths, 3 cm
oral aperture, and normal Atlanto-occipital joint extension. A 20 g intravenous catheter was
inserted and midazolam 2 mg was administered.
In the operating room, standard monitors were applied; the patient was pre-oxygenated with O2
10 L/min for approximately 5 minutes. General anesthesia was induced intravenously with
lidocaine 100 mg, propofol 150 mg, and rocuronium 70 mg. The patient was easily mask
ventilated upon introduction of a 9 mm oral airway. A size 3 Macintosh blade was used to place
a 7.0 mm endotracheal tube (ETT). Placement was confirmed with positive end-tidal CO2
tracing, bilateral breath sounds and equal chest rise it was secured at 22 cm at the lip. An
additional 18g intravenous catheter was inserted. Anesthesia was maintained with 0.5-1 mean
alveolar concentration (MAC) of isoflurane, 50% nitrous oxide and vecuronium. A Brain
Function Monitoring System (BIS by Covidien, Mansfield, MA) was placed to monitor depth of
anesthesia so that volatile gas administration could be minimized.
The patient’s MAP fluctuated from 60-100 mm Hg during the procedure, with a target MAP of
70 mm Hg as requested by the surgeon. The patient received 5% albumin 1 L, normal saline 1 L,
and plasma-lyte 4500 mL administered over 11 hours. Urinary output was 60-300 mL/hr for a
total of 1330 mL. Blood pressure was maintained the first five hours of the case with total bolus
doses of phenylephrine 1080 mcg and ephedrine 165 mg. A phenylephrine infusion was then
initiated for the final 2 hours, totaling 2735 mcg. Seven hours in to the case vasopressin 2 units
IV was administered and no additional vasopressors were required.
At the conclusion of the procedure, neuromuscular blockade was antagonized with neostigmine 3
mg and atropine 0.4 mg IV. Estimated blood loss was 225 mL. The patient demonstrated return
of spontaneous ventilation at 15/min, tidal volumes of 350 mL, and ability to follow commands.
The ETT was removed with positive pressure. The patient was transferred to the post-anesthesia
care unit with O2 10 L/min via facemask, stable vital signs (BP 123/62 mm Hg, MAP 84 mm Hg,
heart rate 88/min, respiratory rate 15/min, SpO2 100%), and a patent airway.
26
Discussion
Anesthetic priorities for a DIEP flap include muscle relaxation, keeping the patient warm and
well hydrated. These interventions minimize peripheral vasoconstriction which could impair
graft perfusion.3 The surgeon also requested a MAP of 70mmHg because hypotension and
vasopressor use causes the vessels to spasm and making anastomosis under a microscope very
difficult. This hemodynamic parameter was antagonized by the patient’s continued ACEI
therapy. Discontinuation of ACEI therapy on the day of surgery is common practice, although
steadfast guidelines are not available.4,5 The American College of Physicians initially
recommended to stop ACEI therapy on the day of surgery and then later modified its
recommendation to continue ACEI with caution in patients with cardiac failure.4 The American
Society of Anesthesiologists (ASA) does not have any guidelines or recommendations regarding
ACEI. In 2012, the ASA’s chair of the committee on regional anesthesia, who is also the clinical
practice chair of the Mayo Clinic’s department of anesthesiology, reported that all Mayo Clinic
surgical patients are requested to hold their ACEI on the day of surgery.5
Blood pressure is regulated by three systems in the body; the sympathetic nervous system, the
renin-angiotensin aldosterone system (RAAS) and the vasopressin system. ACEI’s inhibit the
RAAS. General anesthesia inhibits the sympathetic nervous system so the body is left to
compensate with the vasopressin system.1 Hypotension was evident in our patient even after
induction medication effects had subsided. We started replacing volume using crystalloids with
minimal results and supplemented with IV bolus doses of phenylephrine and ephedrine as
necessary to support her MAP. Colloid administration was our next action in replacing the
volume and avoiding vasopressors. Volume resuscitation was evaluated by urinary output and
anesthetic fluid replacement calculations. Maintenance of 120 mL/hr, deficit of 960 mL and third
space loss of 4 mL/kg/hr was replaced. The patient’s MAP remained in the low 60’s after
adequate volume resuscitation despite titrating the volatile anesthetic to an appropriate BIS
reading and administering multiple ephedrine and phenylephrine boluses. A phenylephrine
infusion was then initiated; 25 mcg/min was required to keep the patient’s MAP near 70 mm Hg.
Phenylephrine and ephedrine are considered first-line agents for treating hypotension during
anesthesia but several studies have shown this therapy is not adequate to treat refractory
hypotension in patients receiving ACEIs.4 At this point, the surgeon was under the microscope
working on anastomosis of the transplanted vasculature. We frequently consulted regarding the
blood pressure and spasm of the vessel. We gave 2 units of Vasopressin IV bolus and for the
remaining three hours of surgery no other vasopressor therapy was needed.
Review of a similar case report identified several risk factors contributing to the patient’s
hypotension: age, use of ACEI on day of surgery, other antihypertensive medications
(metoprolol and chlorthalidone), and administration of propofol at induction.6 Analgesia was
achieved with totals throughout the case of fentanyl 250mcg, acetaminophen 1000mg and
ketamine 40mg. This choice was supported in the literature because ketamine increases heart rate
and blood pressure without causing significant change in autonomic nervous system.4
If a case similar to this presented, alternative anesthetic choices should be considered. Induction
was achieved with 1.8 mg/kg of propofol, the patient had received approximately 200mL of
crystalloid prior. Studies have shown that etomidate or methohexital would be a more
cardiostable agent.4 Also, a dose of 1.3mg/kg of propofol is associated with the least need for
27
pharmacologic intervention to treat bradycardia and hypotension in patients on ACEIs. 7 An
intravenous bolus of 10 mL/kg of crystalloid administered prior to induction has also been shown
to minimize resultant hypotension.4
Comparing maintenance of anesthesia at 0.5 MAC between isoflurane, sevoflurane and
desflurane, little difference is noted in respect to their effects on sympathetic nervous system and
catecholamine levels. Above 0.5 MAC desflurane is associated with higher sympathetic nerve
conduction and higher catecholamine concentrations.4 After initial efforts with ephedrine and
phenylephrine were unsuccessful, norepinephrine could have been considered for its alpha and
beta 1 effects; addressing that a patient on ACEI’s has a lower amount of circulating
catecholamines.4 A reported disadvantage of administration of norepinephrine when compared to
vasopressin is more episodes of hypertension.4 Vasopressin-mediated vasoconstriction is not
attenuated by ACEI therapy as it works independently of the RAAS, and hence why it was
chosen to treat the hypotension refractory to ephedrine and phenylephrine. Alterations in the
induction dose, volatile choice, and vasopressor use could have better optimized the patient’s
blood pressure. The phenylephrine infusion may have been avoided, and perfusion better
supported ultimately avoiding vasospasm of the vasculature and decreasing surgical time.
References
1. Thoma A, Pathophysiology and management of angiotensin-converting enzyme inhibitorassociated refractory hypotension during the perioperative period. AANA J. 2013;81(2):133140. PMID:23971233
2. Rosenman D, McDonald F, Ebbert J, Erwin P, LaBella M, Montori V. Clinical consequences
of withholding versus administering renin-angiotensin-aldosterone system antagonists in the
preoperative period. J Hosp Med. 2008;3(4):319-325. doi:10.1002/jhm.323.
3. Chang J, Kahn D, Lim A, Cornaby T. Plastic and reconstructive surgery. In Jaffe RA,
Samuels SI, eds. Anesthesiologist’s manual of surgical procedures. 4th ed.
Philadelphia:Lippincott Williams & Wilkins;2009:1131-1137.
4. Mets B. Management of hypotension associated with angiotensin-axis blockage and general
anesthesia administration. J Cardiothorac Vasc Anesth. 2013;27(1):156-167.
doi:10.1053/j.jvca.2012.06.014.
5. Bogebjerg M. No consensus on withholding angiotensin-converting enzyme inhibitors and
angiotensin receptor blockers before spinal anaesthesia. Dan Med J. 2012;59(12)A4543.
PMID:23290284.
6. Srivastava K, Sacher V, Nelson C, Lew J. Multifactorial model and treatment approaches of
refractory hypotension in a patient who took an ACE inhibitor the day of surgery. Case Rep
Anesthesio[serial online]. 2013. doi:10.1155/2013/723815.
7. Weisenberg M, Sessler D, Tavdi M, et al. Dose-dependent hemodynamic effects of propofol
induction following brotizolam premedication in hypertensive patients taking angiotensinconverting enzyme inhibitors. J Clin Anesth. 2010;22(3):190-195.
doi:10.1016/j.jclinanes.2009.07.008.
Mentor: Courtney Brown, CRNA, PhD
28
Anesthetic Management of Mitral Valve Prolapse
Jason E. Goodin, BSN
Wake Forest Baptist Health
Keywords: mitral valve, prolapse, regurgitation, leaflets, valvular disease
Anesthetic considerations related to mitral valve prolapse depends on the severity of the disease
and the patient’s self-report of symptoms. Mitral valve prolapse (MVP) is defined as the upward
movement of one or more of the leaflets during systole, regurgitant flow may or may not be
present.1 This cardiac abnormality receives less attention compared to other valvular defects, but
it is the most common valve disease, affecting up 2.5% of the healthy population.2 To safely treat
patients diagnosed with mitral valve prolapse (MVP), the underlying symptoms and disease
severity should be known prior to implementing an anesthetic plan.
Case Report
A 68-year-old, 80 kg female with five year history of lower back pain and leg numbness, was
scheduled for a posterior lumbar interbody fusion of L3-5. Additional medical history included:
diabetes mellitus type II, hypertension, hypothyroidism, splenic aneurysm, and mitral valve
prolapse with mild regurgitation. At the time surgery, there were no echocardiogram results and
a recent EKG showed sinus rhythm. Of note the patient was prescribed a daily fentanyl patch for
control of chronic pain related lumbar disc disease.
A pre-anesthesia assessment and physical examination was performed, and the patient was noted
to have a Mallampati class 3, thyromental distance and oral aperture of 3 finger breadths.
Laboratory work was remarkable for anemia with a hemoglobin of 9 g/dL and hematocrit of 30
g/dL. The anesthetic plan was discussed with the patient and informed consent was obtained. A
general anesthetic was planned for the procedure with a kneeling prone surgical position.
An 18 gauge peripheral IV was placed in the holding room with a slow infusion of normal saline.
Midazolam 1 mg was administered, and the patient was transported to the operating room. The
patient remained on the stretcher for induction, and all standard monitors were placed. Oxygen
was administered via face mask at 10 L/min until expired O2 concentration was greater than
80%.
Once adequate pre-oxygenation was achieved, the patient was induced with intravenous:
lidocaine 80 mg, propofol 160 mg, fentanyl 100 mcg, and rocuronium 50 mg. Phenylephrine in
the amount of 720 mcg was given post induction to maintain blood pressure within 20% of
baseline. Elective use of an endotracheal light wand was used to place a 7.0 ETT due to patient’s
body habitus and airway exam. Final surgical position was prone with use of chest rolls and
ProneView (Dupaco, Inc., Oceanside, CA). Adequate padding was used on all pressure points.
Anesthesia was maintained with a fentanyl infusion which was discontinued 1 hour prior to
closure, isoflurane at 0.8% inspired concentration with 1 L/min flow of nitrous oxide and O2, and
rocuronium boluses. At the start of closure, 5 mg of neostigmine along with 1 mg of
glycopyrrolate was given to adequately antagonize the neuromuscular blockade. The patient was
29
returned to supine position on the stretcher. The patient achieved adequate tidal volumes,
responded to verbal command, and the endotracheal tube was removed. The patient maintained a
patent airway with stable vital signs, and was transported PACU on supplemental oxygen. A
total of 1 L of normal saline and 1.2 L of plasmalyte was given during the procedure. Blood loss
was estimated at 200 mL. Report was given in PACU, and the patient remained in the hospital
overnight for observation.
Discussion
Mitral valve prolapse (MVP) can occur in patients with no prior, related medical history. The
presence is often benign, showing no symptoms.3,4 Females have a higher incidence of the
disease, as do patients with a history of rheumatic fever, myocarditis, lupus, and Marfan
syndrome.1 Patients may be asymptomatic or suffer from cardiac dysrhythmias, dyspnea, or
fatigue.3 These symptoms typically will vary with the severity of the prolapse and whether or not
regurgitant flow is present.4 A person with severe mitral valve prolapse may have similar
symptoms as someone with mitral valve insufficiency such as cough, fatigue, shortness of breath,
and chest palpitations.3 Surgical correction is often considered once dyspnea is present with
moderate to severe regurgitant flow through the valve.1,2 More severe cases pose potential
serious complications such as embolic stroke, congestive heart failure, lethal dysrhythmias, and
cardiac sudden death.1
Patients may be diagnosed with mitral valve prolapse by expressed symptoms or a mid-systolic
murmur heard by auscultation.1 A definitive diagnosis is made by transesophageal
echocardiography, which observes mitral valve movement during the cardiac cycle.4,5 An
echocardiogram can also help visualize flow dynamics, determine if any regurgitant flow is
present, and provide information to accurately diagnose the severity of the condition and proceed
with the appropriate treatment.5,6
The anesthesia practitioner should have a general overview of optimal physiologic conditions for
patients with mitral valve prolapse.1,6 A baseline or recent EKG will help define the presence of
frequent premature ventricular complexes and/or QT interval changes possibly related to MVP.2
Previous studies indicate that reducing left ventricular (LV) preload will increase the amount
mitral valve prolapse, thus increasing the regurgitant flow.4 Anesthetic considerations should
include; maintaining systemic vascular resistance (SVR) at or near the patient’s baseline level,
avoiding increasing cardiac contractility, attenuating changes in heart rate and ensuring a
euvolemic volume status.1,7 Volume overload or fluid depletion could increase symptoms in a
patient with MVP by altering LV preload.4,7 The sitting or Trendelenburg surgical positions can
also decrease LV filling and should be avoided if possible.4
Additional equipment, such as an arterial line, a foley catheter, and a pulmonary artery catheter
may serve as useful tools to monitor SVR and volume status during surgery.1,4 Volatile and
intravenous anesthetics are safe to use with MVP as long as the dose is titrated to avoid
prolonged hypotension.4 Systemic hypotension may be treated with phenylephrine to increase
SVR. Previous research suggests to avoid drugs, such as ketamine and desflurane that can
increase a sympathetic cardiac response.4 Increasing heart rate and contractility can exacerbate
symptoms of MVP; therefore, drugs that mimic this response should be avoided.1,4 Opioids are
30
also an appropriate choice for these patients due to the blunted sympathetic response, lack of
cardiac depression, and decreased reaction to surgical stimulus they provide.1,7
In the case presented, adequate volume resuscitation was used to maintain an appropriate volume
status and counteract intraoperative blood loss as well as initial fluid deficit. In addition, the
patient was appropriately treated with opioid analgesia to decrease the sympathetic response
caused by direct laryngoscopy and surgical incision. Prior to surgery, the patient was on an
opioid regimen at home; therefore, opioids were tolerated well and liberally administered to
maintain appropriate analgesia. Phenylephrine was given post induction to counteract
hypotension associated with the anesthetic initiation. Conscientious attention was given to blood
pressure and fluid management to avoid drastic changes from baseline status. Maintaining
hemodynamics and fluid volume was aimed at preventing any additional MVP or altering
cardiac output status associated with the anesthetic. The patient’s hemodynamics were stable
during the remainder of the case with no signs of cardiac instability. The patient was required to
be in the kneeling, prone position for surgery, which did not appear to cause any hemodynamic
alterations or present issues with the anesthetic plan. The kneeling prone position is known to
sequester blood in the lower extremities and increase intra-abdominal pressure which leads to a
decrease in cardiac preload. Overall, the procedure was tolerated well by the patient without any
intra- or post-operative sequelae.
Patients with MVP can safely undergo surgical procedures with general anesthesia; however,
caution and appropriate technique must be employed by the anesthesia practitioner to protect
patients from possible complications related to the anesthetic. Prior to surgery, planning and
discussion by the anesthesia team will reduce risks and provide optimal operative conditions for
the patient. Anesthesia professionals should follow current practice guidelines and apply the
appropriate monitors during surgery to reduce risks, while also educating the patient how their
condition relates to the anesthetic plan.
References
1. Herrera A. Valvular heart disease. In: Stoelting R, Hines R, Marschall K. Stoelting's
Anesthesia and Co-Existing Disease. 5th ed. Philadelphia: Saunders/Elsevier; 2012:34-36.
2. Gewillig M, Werner B, Flameng W. Mitral valve prolapse. SA Heart. 2007;4(4):14-20. 3. Chen M. Mitral valve regurgitation. US National Library of Medicine. 2015. Available at:
http://www.nlm.nih.gov/medLineplus/ency /article/000176.htm. Accessed June 12, 2014.
4. Wallace A. Cardiovascular disease. In: Miller R, Pardo M, Stoelting R. Basics of Anesthesia.
6th ed. Philadelphia, PA: Elsevier/Saunders; 2011:396-397.
5. Lee AP, Hsiung MC, Salgo IS, et al. Quantitative analysis of mitral valve morphology in
mitral valve prolapse with real-time 3-dimensional echocardiography: Importance of annular
saddle shape in the pathogenesis of mitral regurgitation. Circulation. 2013;127(7):832-41.
6. Vernick WJ, Woo JY. Anesthetic considerations during minimally invasive mitral valve
surgery. Semin Cardiothorac Vasc Anesth. 2012;16(1):11-24.
7. Reckard D, Cipcic E, Mackin C. Mitral valve replacement: A case report. AANA J.
2008;76(2):125-129. Mentor: Courtney Brown, CRNA, PhD 31
Converting to General Anesthesia in a Complex Parturient
Michael Murphy, MS
Northeastern University
Keywords: Obstetric anesthesia, granulosa cell tumor, cesarean section, general anesthesia,
American Society of Anesthesiologists (ASA) Practice Guidelines for Obstetrical Anesthesia
Neuraxial anesthesia is frequently the anesthetic method of choice for cesarean sections due to
the airway and respiratory changes associated with pregnancy. However, a general anesthetic
may be required due to a neurologic or coagulation disorder, inadequate dermatome coverage, or
procedure urgency. Fortunately, epidural anesthesia may be re-dosed when utilized, however, the
incidence of failed neuraxial anesthesia during cesarean sections thus necessitating conversion to
general anesthesia is reported at 1.7%1 General anesthesia offers benefits during obstetrical
emergencies, yet can pose risks, including the significant incidence of 1/533 failed intubations.1
With updated algorithms, expert anesthesia professionals, and availability of advanced airway
devices, general anesthesia can be safe for both mother and fetus.1
Case Report
A 30-year-old gravida 1 at 41 weeks’ gestation underwent induction with an epidural for labor
analgesia. The patient was 170 cm tall and weighed 105.5 kg. The patient’s medical history
included a documented vicodin allergy, left ovarian cyst, pancreatitis, and a history of
chemotherapy for stage II granulose cell tumor of the right ovary from one year prior. During her
pregnancy, a questionable pelvic cyst was noted on ultrasonic imaging demonstrating
characteristics consistent with ovarian granulosa cell tumor (OGCT). The patient’s current
medication regime consisted solely of prenatal vitamins. Laboratory values upon admission
included: hemoglobin 10.7 g/dL, hematocrit 31.2 %, platelets 154,000/μL and chemistries within
normal limits.
When she progressed to 9 cm dilation, the baby began to demonstrate reduced variability and late
decelerations on fetal monitors. The patient was immediately brought to the operating room for
emergency cesarean section. An18-gauge peripheral intravenous catheter was in place. The
patient’s airway was classified as Mallampati II. The initial anesthesia plan consisted of utilizing
the previously placed epidural with a lidocaine 2% bolus of 20 ml. A T4 dermatome level was
obtained with the epidural bolus and augmented with fentanyl 100 mcg, which provided
sufficient coverage for incision. Upon arrival to the operating room, oxygen was administered
via nasal cannula at 4 L/min, standard monitoring initiated. The patient was placed in left uterine
displacement. The patients’ vital signs at this time were HR: 86, BP: 123/80, SpO2: 98%. Upon
delivery, oxytocin 20 U/L was initiated with an estimated blood loss of 1000 ml. The obstetrician
explained to the patient and the anesthesia providers the need for oncology to assist with
debulking a pelvic tumor. As the surgical procedure progressed, the patient complained of
increasing discomfort. Instead of rebolusing the epidural, intravenous anesthesia was utilized.
However, the patient’s discomfort was refractory to multiple administrations of ketamine and
fentanyl, totaling 50 mg and 100 mcg, respectively. As the laparotomy progressed, a
32
hemorrhagic mass versus hematoma in the posterior cul-de-sac was found. The patient,
anesthesia providers and the surgical team decided to convert to a general anesthetic due to the
increased possibility of hemorrhage and insufficient dermatome coverage provided by the
epidural. A rapid sequence induction (RSI) with cricoid pressure was performed using fentanyl
100 mcg, propofol 150mg and succinylcholine 100 mg. Direct laryngoscopy with a Miller #2
blade was performed and resulted in a grade I view of the glottis. The airway was secured
without difficulty with a #7 endotracheal tube. General anesthesia was maintained during the
case with sevoflurane 1.8% inspired concentration in a mixture of oxygen 2 L/min and nitrous
oxide 2 L/min. An additional large-bore intravenous and arterial line were established and the
remaining two-and-a-half-hour surgical time was focused on tumor debulking, hemostasis
maintenance, and abdominal closure. An additional administration of oxytocin 20 U/L was hung
and five liters of normal saline were infused to maintain the patient’s blood pressure throughout
the case. Despite the increased blood loss, totaling 1800 ml, the bedside hemoglobin levels were
8.0 g/dl. The remainder of the surgery progressed uneventfully. The patient was extubated and
transferred to the post anesthesia care unit, alert and hemodynamically stable.
Discussion
Currently, the ASA Task Force on Obstetrical Anesthesia recommends epidural or spinal
anesthesia over general anesthesia for cesarean sections. While time from anesthesia start to
delivery is shortest with general anesthesia, maternal and fetal complications increase.2
Neuraxial anesthesia decreases maternal stress, improves patient satisfaction, and provides
sufficient pain relief during labor.3 The benefits of neuroaxial anesthesia over GA for cesarean
section are due to limited drug transfer to the fetus, and the respiratory/airway changes
associated with pregnancy.1
As with all anesthetic plans, cesarean deliveries should include possible conversion to general
anesthesia. It requires advanced planning, even for experienced obstetric anesthesia practitioners,
to safely manage an emergency conversion.4 The complex physical alterations in pregnant
women can create additional challenges when providing general anesthesia to this patient
population. The case study presented above reflects the suggested ASA guidelines when
requiring conversion to general anesthesia.2
This patient’s medical history supplied an additional obstacle, making a conversion to general
anesthesia much more likely. OGCT are rare, accounting for only 2-5% of all ovarian
neoplasms.5 These tumors are described as slow growing, with a later incidence of reoccurrence.
Reoccurrence ranges have been documented from five to thirty years, with an overall
unfavorable prognosis.5 There are currently no standard guidelines for OGCT, however,
improved outcomes have been achieved with surgical debulking combined with chemotherapy.
In this case, an initial plan was established for standard vaginal delivery, yet, if a cesarean
section proved necessary, the surgical team had obtained consent for an exploratory laparotomy.
With the expanded scope of this surgery and inadequate dermatome coverage, general anesthesia
with an RSI was our choice. Since parturients are considered to have full stomachs, and are at an
increased risk of aspiration, a rapid sequence induction is the preferred method to secure the
airway.2 There are reports of an increase in difficult intubations in term parturients, upwards of
33
16%; the risk of failed intubations is at least 10 times greater in parturients as compared to the
general surgical population.6 The rapid change in anesthetic plan was made in accordance with
current guidelines and standards.2 Conversion to general anesthesia was made with the foresight
that the patient could be a difficult intubation. Advanced airway devices, including a bougie and
Glidescope (Verathon Inc., Bothell, WA) were readily available, but were not utilized for the
case. A recent observational study of 5,000 general anesthetics on pregnant women did not note
any incidence of aspirations.1 The results of this study, however, do not reject the possibility of
an aspiration occurring. Given the myriad of complications, anesthesia providers should weigh
the risks associated with general anesthesia in order to best maintain a secure airway.
With the increased possibility of blood loss necessitating rapid fluid administration, a second
large-bore intravenous was established. Current literature has yet to address central venous
access use alone for obstetrical patients. Yet, recommendations provided by the ASA suggest
large-bore access when hemorrhagic emergencies are encountered.2 Additionally, current
recommendations provided by the ASA suggest invasive hemodynamic monitoring should be
initiated individually based on clinical presentation.2 Given the increased surgery scope, an
arterial line was inserted to monitor the patient’s hemodynamics, as well as to obtain blood
specimens.
Parturients experience a hemodilutional anemia due to increased plasma levels, along with
slightly increased hemoglobin. This relative anemia rarely requires a blood transfusion given the
increased circulating volume. Particularly with this patient’s hemoglobin of 8.0 G/dl, blood
transfusion was not required to improve the patient’s oxygen carrying capacity. The patient
likely experienced some extent of hemodilution, considering the amount crystalloid
administered. Significant post-partum hemorrhage occurs in <1% of all deliveries.7 Research
also demonstrates a hemoglobin level of 7.0 G/dl is the cut off to provide sufficient oxygen
carrying capacity in healthy women.7 Expected estimated blood loss for cesarean section can
reach upwards of 1000 ml. As the case progressed, there was a reduction in blood loss rate and
hemostasis was adequate, thus a coagulation panel was not deemed necessary.
Neuraxial anesthesia can sufficiently blunt the noxious stimuli of a cesarean section. However,
this case demonstrates the need for constant vigilance, communication with the patient and
surgical team, and preparation for immediate conversion to general anesthesia, when neuraxial
anesthesia is not sufficient. With the infrequent need for general anesthesia in this unique patient
population, the risks and complexities may not be familiar to anesthesia providers. It is necessary
for anesthesia providers to be aware of complications associated with obstetrical anesthesia and
to plan ahead to avoid them, as well as maintain flexibly to safely adapt as patients' needs vary.
With the rare complexities of this case the conversion from neuraxial to general anesthesia was
the appropriate decision and was managed according to current recommendations based upon
best evidence.
Reference
1. D'Angelo R, Smiley RM, Riley ET, Segal S. Serious complications related to obstetric
anesthesia: the serious complication repository project of the Society for Obstetric
Anesthesia and Perinatology. Anesthesiology. 2014;120(6):1505-1512.
34
2. American Society of Anesthesiologists Task Force on Obstetric A. Practice guidelines for
obstetric anesthesia: an updated report by the American Society of Anesthesiologists Task
Force on Obstetric Anesthesia. Anesthesiology. 2007;106(4):843-863.
3. Gizzo S, Noventa M, Fagherazzi S, et al. Update on best available options in obstetrics
anaesthesia: perinatal outcomes, side effects and maternal satisfaction. Fifteen years
systematic literature review. Arch Gynecol Obstet. 2014;290(1):21-34.
4. Ortner CM, Richebe P, Bollag LA, Ross BK, Landau R. Repeated simulation-based training
for performing general anesthesia for emergency cesarean delivery: long-term retention and
recurring mistakes. Int J Obstet Anesth. May 4 2014.
5. Al-Badawi IA, Abu-Zaid A, Azzam A, AlOmar O, AlHusaini H, Amin T. Cytoreductive
surgery and hyperthermic intraperitoneal chemotherapy for management of
recurrent/relapsed ovarian granulosa cell tumor: a single-center experience. J Obstet
Gynaecol Re. 2014;40(9):2066-2075.
6. Balki M, Cooke ME, Dunington S, Salman A, Goldszmidt E. Unanticipated difficult airway
in obstetric patients: development of a new algorithm for formative assessment in highfidelity simulation. Anesthesiology. 2012;117(4):883-897.
7. Ickx BE. Fluid and blood transfusion management in obstetrics. Eur J Anaesth.
2010;27(12):1031-1035.
Mentor: Janet A. Dewan, CRNA, PhD
Negative Pressure Pulmonary Edema in a Pediatric Patient
Christine DePasquale Calder, MS
Northeastern University
Keywords: Negative pressure pulmonary edema, post-operative pulmonary edema, postobstructive pulmonary edema, obstructive sleep apnea, tonsillectomy
Negative pressure pulmonary edema (NPPE) or post-operative pulmonary edema (POPE) can
rapidly become a life-threatening anesthetic emergency. The presentation of NPPE can be
immediate or delayed and can be confused with other causes of postoperative respiratory
distress. The disorder has been classified into 2 types, each with similar clinical pictures, but
with differing etiology. Type I follows a sudden severe episode of upper airway obstruction
(UAO) such as laryngospasm, while Type II develops after relief of a chronic obstruction such as
enlarged tonsils or upper airway tumor.1 This report details a case of respiratory distress in a
pediatric patient following tonsillectomy
Case Report
A 5-year-old male, measuring 39 kg in weight and 110 cm in height, presented for tonsillectomy
and adenoidectomy. His past medical history included chronic otitis media, obstructive sleep
apnea (OSA), enlarged tonsils, and chronic upper respiratory infections. A sleep study evaluation
revealed an apnea-hypopnea index (AHI) of 6. Past surgical history included bilateral
35
myringotomy and tube insertion. The patient’s medications included albuterol metered dose
inhaler, 2 puffs every 6 hours, as needed. Three weeks prior to admission, he completed a 7 day
course of amoxicillin/clavulanic acid for reoccurring sinusitis and otitis media. On physical
examination, breath sounds were clear to auscultation and clear nasal drainage was noted. The
patient’s mother reported that he was free of any recent cough or fever. Assessment of the airway
revealed a Mallampati score of I, normal dentition, and 2+ tonsillar hypertrophy. The patient had
nothing by mouth for 8 hours prior to surgery. He received acetaminophen 10mg/kg orally in the
pre-operative unit.
Accompanied by his mother, the patient was taken to a pre-warmed operating room and placed
supine on the operating table. A pulse oximetry monitor was applied and a mask induction was
initiated with a blend of 3 L of oxygen, 6 L of nitrous oxide, and 8 % sevoflurane. Once
induction of anesthesia was accomplished, the mother was escorted from the room. Standard
monitors were applied and the eyes were taped. A 22-gauge peripheral intravenous (IV) catheter
was inserted in the left hand. Propofol 50mg and fentanyl 30 mcg were administered through the
IV. The nitrous oxide was discontinued and the patient's trachea was intubated under direct
laryngoscopy with a Miller 2 blade and a 5.0 mm cuffed oral endotracheal tube (ETT). Clear,
thick post-nasal secretions were noted during laryngoscopy. Placement of the ETT was
confirmed by the presence of end tidal carbon dioxide (etCO2) and bilateral breath sounds.
General anesthesia was maintained with 2.5% end-tidal sevoflurane with 1L/min air and 1L/min
of oxygen. The patient was mechanically ventilated on volume control with a respiratory rate of
20 breaths per minute and a tidal volume of 250mL. The temperature was monitored through an
axillary probe. A forced air lower body warming unit was applied.
The surgery was uneventful with the patient’s SpO2 in the range of 99-100% throughout and
blood loss was estimated at 100 ml. Upon return of spontaneous breathing, 1.6 mg of morphine
sulfate was titrated in 0.2mg IV incremental boluses according to respiratory rate. At the
conclusion of the procedure, the surgeon inserted a 16 French orogastric tube (OGT) and
suctioned a moderate amount of bloody secretions. Following this, the oropharynx was suctioned
by the anesthesia professional using a yankauer tonsil tip catheter and a 70 mm oral pharyngeal
airway was inserted. The patient was suctioned a third time with a Y-suction catheter through
the oral airway to remove thick yellow secretions. The ETT was removed from the trachea with
the patient breathing spontaneously at a rate of 15 breaths per minute and in a deep plane of
anesthesia expiring 3.4 % end tidal concentration of sevoflurane in 3 L/min of oxygen.
Following extubation, the patient continued to spontaneously breath with no signs of obstruction,
and was transported to the post anesthesia care area (PACU) with a face-mask of oxygen at 8
L/min.
Upon arrival in the PACU, the SpO2 was 96%. Auscultation of the lungs revealed coarse lung
sounds. He was suctioned through the oral airway and yellow secretions were again removed.
Upon awakening and approximately 15 minutes after arriving in the PACU, the patient was
restless, and SpO2 was 92%. Breath sounds continued to sound coarse and a chest radiograph
was ordered. A face-mask was applied and humidified oxygen was administered at 6 L/min. The
SpO2 continued to stay at 92% for about 15-20 minutes and began to slowly trend up to 94%.
After approximately 30-45 minutes, the PACU anesthesia physician and surgeon decided to
36
admit the patient for observation based upon symptoms. He was discharged 24 hours later with
no complications and an unremarkable chest radiograph.
Discussion
Obstructive sleep apnea (OSA) occurs when the upper airway is obstructed in some way during
sleep, which causes “repetitive arousal from sleep to restore airway patency, which may result in
daytime hypersomnolence or other daytime manifestations of disrupted sleep…”.2 It can result
in episodes of hypercarbia and oxygen desaturationswhich can compromise cardiac function.
Common signs of OSA include a history of snoring, frequent somnolence despite adequate sleep
time, and pauses in breathing or a choking sensation during sleep.3 Conditions associated with
OSA include obesity, hyperplasia of the tonsils and adenoids, muscular dystrophy, Down
syndrome, and craniofacial abnormalities.2
This case report describes an example of respiratory distress following tonsillectomy and
adenoidectomy in a pediatric patient with a history of OSA. Patients with a history of enlarged
tonsils and OSA are at risk for developing NPPE, Type II following surgical relief of the upper
airway obstruction. A review of the pathophysiology, clinical manifestations, differential
diagnosis and management of patients manifesting signs of Type I and Type II NPPE will be
presented.
The pathogenesis of NPPE is multifactorial and related to disturbances of one of four
mechanisms: increased hydrostatic pressure in the pulmonary capillary bed, decreased osmotic
pressure of plasma, increased permeability of the membrane, and decreased return of fluid to the
circulation by way of the lymphatics.1 The predominant mechanism is forced inspiration against
a closed glottis inducing a negative gradient of intrapleural and transpulmonary pressure.
In children, normal intrathoracic pressure is -2.5 to -10 cmH2O; however, breathing against an
obstructed airway can create a large negative intrathoracic pressure (>-30cmH2O).3 The high
pressure gradient causes the transudation of fluid from the pulmonary vessels into the interstitial
spaces and alveoli of the lungs, resulting in pulmonary edema.4 When a large amount of fluid
enters the interstitial compartment, alveoli flooding occurs. The marked increase in intrapleural
negative pressure leads to increased venous return to the right ventricle. The result is decreased
left ventricular output leading to an elevation in pulmonary blood volume and microvascular
pressure. The increased volume and pressure in the right ventricle causes distension of the
septum into the left ventricle. This results in a decrease in compliance, increase in workload and
increase in end diastolic and end systolic ventricular volumes.1 In addition, lack of alveolar
oxygenation during the obstruction results in hypoxemia. The result is a hyperadrenergic state.
Peripheral vasoconstriction shunts blood centrally. Damaged pulmonary capillaries exhibit
increased permeability and hypoxia-mediated pulmonary vasoconstriction all of which favor the
formation of pulmonary edema.1
NPPE is categorized as Type I or Type II. Type I occurs directly after an acute upper airway
obstruction, commonly from laryngospasm. The etiologies for Type I are strangulation, upper
airway tumors, epiglottitis, croup, ETT obstruction, and mononucleosis.1 The cause of Type II is
less clear. It develops in patients when a chronic upper airway obstruction (UAO) such as
37
hypertrophic tonsils and adenoids or upper airway tumor is removed.1 In Type II NPPE, it is
postulated that UAO leads to a ball valve effect, whereby large positive intrathoracic pressures
are generated. It is thought that the obstruction may actually limit the fall in oxygen saturation
and transpulmonary capillary pressure as the result of positive end-expiratory pressure (PEEP) it
creates. Once the obstructive tonsils or mass are removed, PEEP disappears. Venous return then
increases, along with pulmonary blood volume and pulmonary hydrostatic pressure, creating a
negative intrapulmonary pressure and transudation of fluids into interstitial space and alveoli of
lungs.1 The incidence of Type I NPPE developing with acute postoperative upper airway
obstruction is 9.6–12%; for Type II NPPE the rate of manifestation is 44%. 1 In adults, 50% of
the NPPE cases are a result of post-operative laryngospasm.1
Symptoms of NPPE can develop rapidly after extubation or can be delayed a few hours due to
the positive pressure created by the patient expiring against a closed glottis. Therefore, a patient
at risk must be observed in the PACU for an extended period of time. The initial clinical
presentation usually includes decreased oxygen saturation, pink frothy sputum, wheezing, and
chest radiograph with diffuse infiltrates.3 Signs of acute airway obstruction include stridor, use of
accessory muscles for inspiration and retractions, tachypnea, tachycardia, secretions, and a an
expression of panic.1 On auscultation, crackles and wheezes can be heard. Hypoxemia is the
result of impaired diffusion of oxygen and ventilation/perfusion mismatching.1
This patient presented in this case report was admitted for observation because he was showing
early signs and symptoms consistent with NPPE, Type II. This patient had a history of OSA with
an AHI of 6, which is considered mild to moderate OSA, and suggests need for surgical
treatment. This put him at risk for development of NPPE.2
The initial management for patients exhibiting NPPE is oxygen therapy, correction of the
hypoxemia, and removal of the airway obstruction.1 Oxygen administration can be supplied with
5-10 cmH2O of PEEP or continuous positive airway pressure to resolve the pulmonary edema.5
In some severe cases of NPPE, intubation with an ETT and 100% oxygen mechanical ventilation
is needed. Diuretics to decrease the intravascular volume are controversial because it can cause
hypovolemia and hypotension in post-surgical patients.5 According to Bhaskar, “NPPE resolves
generally within 24 h. However, when recognition is delayed, patients with NPPE have mortality
rates ranging from 11% to 40%.”1
Currently, there are no measures to accurately predict a child's risk for developing NPPE after
the obstruction is corrected.3 However, to decrease the risk, the anesthesia professional should
take measures to avoid laryngospasm by assuring adequate anesthesia during mask ventilation or
deep extubation, or ensure a patient is fully awake with adequate airway function prior to
extubation.5 This patient was adequately anesthetized for a deep extubation with an end-tidal
sevoflurane concentration of 3.4%, along with no changes in heart rate or cough with oropharynx
suctioning. His airway was clear after extubation and he did not exhibit laryngospasm. The
patient was admitted for observation due to an awake SpO2 of 92% on oxygen, coarse lung
sounds and a history of OSA. Symptoms resolved in less than 24 hours.
38
References
1. Bhaskar B, Fraser JF. Negative pressure pulmonary edema revisited: pathophysiology and
review of management. Saudi J Anesth. 2011:5(3)308-313.
2. Gross JB, Bachenberg KL, Benumof JL, et al. Practice guidelines for the perioperative
management of patients with obstructive sleep apnea. Anesthesiology. 2006;104:1081-93.
3. Ferrari LR, Nargozian C. Anesthesia for otolaryngologic surgery. In: Barash PG, Cullen BF,
Stoelting RK, Cahalan MK, Stock MC, Ortega R, ed. Clinical Anesthesia 7th ed.
Philadelphia, PA:Wolters Kluwer/Lippincott Williams & Wilkins; 2013:1360-1361.
4. Oron Y, Marom T, Russo E, Ezri T, Roth Y. Don’t overlook the complications of
tonsillectomy. The J Fam Practice. 2010;59(10):E4-E9.
5. Udeshi A, Cantie SM, Pierre E. Postobstructive pulmonary edema. J Crit Care.
2010;25:508e1-508e5.
Mentor: Janet A. Dewan, CRNA, PhD
Anesthetic Implications for a Patient with Gitelman’s Syndrome
Jamie Greicar, MN
University of North Dakota
Keywords: Gitelman’s syndrome, metabolic acidosis, Bartter’s syndrome, renal tubular disorder
Gitelman’s syndrome (GS), first described in 1966 and also referred to as Gitelman’s variant of
Bartter’s syndrome, affects an estimated 1 in 40,000 people worldwide.1 GS is a congenital,
autosomal recessive, renal tubular disorder, characterized by chronic hypokalemia,
hypomagnesemia, and hypocalciuria associated with metabolic alkalosis and normal blood
pressure. During routine anesthesia care, the metabolic acidosis associated with GS can be
further exacerbated by preoperative fasting, anesthetic medications, endotracheal intubation and
controlled respirations, and intraoperative fluid and electrolyte management.1 Without proper
anesthetic planning and strict patient monitoring, GS can precipitate perioperative respiratory,
cardiovascular, musculoskeletal, and neurologic complications.
Case Report
A 37-year-old, 160 cm, 62.7 kg, female presented for urgent laparoscopic cholecystectomy
following acute cholecystitis with cholelithiasis. The patient’s medical history was significant for
GS and chronic hypokalemia. Her surgical history included functional endoscopic sinus surgery
under general anesthesia. Her medication regimen included amiloride hydrochloride and
potassium chloride. A preoperative electrocardiogram (ECG) showed normal sinus rhythm with
a heart rate of 78 beats/minute, a PR interval of 0.17 seconds, a QRS interval of 0.09 seconds, a
QT interval of 0.48 seconds, and regular ST segments. Preoperative blood pressure was 97/60
mm Hg, heart rate was 72 beats/min and potassium level was 2.9 mEq/l.
39
On arrival to the operating room, the patient was given intravenous (IV) midazolam 2 mg and
noninvasive monitors were applied. Pre-oxygenation was initiated with O2 flows at 6 L/min via
face mask. IV induction was achieved with fentanyl 100 mcg, lidocaine 50 mg, propofol 150 mg,
and rocuronium 40 mg. The trachea was intubated and placement was confirmed with positive
end-tidal CO2 and auscultation of bilateral breath sounds. The patient was then placed on
synchronized intermittent mandatory ventilation.
Anesthetic maintenance included an expired sevoflurane concentration of 2% with 1.5 L/min of
O2 and 1.5 L/min of air. The patient was given acetaminophen 1000 mg and three fentanyl 50
mcg boluses for procedural pain control. Dexamethasone 10 mg and ondansetron 4 mg were
given prior to incision. Abdominal insufflation was initiated without complication, and
trendelenburg positioning was utilized for increased laparoscopic visualization. ECG was
continually monitored and consistently correlated to preoperative baseline measurements. An
additional 10 mg of rocuronium was used for muscle relaxation during the procedure. A total of
1500 ml of Lactated Ringer’s (LR) was given.
Following completion of the procedure, neuromuscular blockade was antagonized with
neostigmine 3 mg and glycopyrrolate 0.4 mg. When extubation criteria were met the oropharynx
was suctioned and the endotracheal tube was removed without complications. 6 L O2 via simple
mask was utilized with SpO2 98%. Transfer to the recovery room was uneventful and vital signs
remained stable.
Discussion
GS is typically diagnosed in adolescence and early adulthood when symptoms such as muscle
weakness, cramping, spasms, tetany, and/or fatigue present along with laboratory abnormalities
such as metabolic alkalosis and hypokalemia.1 GS is associated with distal convoluted tubule
defects, and has been linked to loss of function in the thiazide sensitive Na-Cl cotransporter
(TSC or NCCT).2 The NCCT is responsible for reabsorption of Na-Cl across the basolateral
membrane of renal intraluminal cells. Patients with defective NCCTs experience salt wasting,
which eventually leads to hypovolemia and metabolic alkalosis.2 Etiology of the NCCT
dysfunction is controversial, but in 1996 Simon et al3 first displayed a variety of nonconservative
amino acid substitutions and splice site mutations on chromosome 16q13 of the NCCT gene.
Since then, more than 140 mutations of the NCCT gene (SLC12A3) have been described.3
The management of GS patients undergoing general anesthesia is complex due to the many
pathophysiologic changes. It is imperative for the Certified Registered Nurse Anesthetist
(CRNA) to consider these changes as they relate to cardiac monitoring, impaired vascular tone,
fluid volume management, electrolyte monitoring and replacement, and medication management.
Potassium and/or magnesium depletion occurring in GS can lead to prolonged action potential
duration of a cardiac myocyte, thus increasing the QT interval on ECG. A prolonged QT interval
will increase the risk for developing ventricular arrhythmias, which could advance to syncope
and sudden cardiac death.4 The case study patient had a decreased potassium level upon
admission, and had a slightly increased QT interval on initial ECG. Her acute cholecystitis could
have further exaggerated the decreased potassium, sodium, chloride, and magnesium levels.
40
Subsequently, there was the potential for further metabolic alkalosis and QT interval
prolongation. The preoperative ECG obtained was compared with intraoperative and
postoperative ECG tracings to monitor for acute changes. Also, preoperative and postoperative
blood draws were completed to strictly monitor electrolyte status.
Patients with GS typically present with a decreased intravascular fluid volume, reduced
peripheral vascular resistance, and normo to hypotension.1 This normotension to hypotension is
consistent despite activation of the Renin-Angiotensin-Aldosterone System (RAAS) by
decreased sodium levels. Activation of the RAAS typically leads to hypertension through
angiotensin II signaling throughout the body, yet this system is overcome by the salt wasting
associated with GS.5 The decrease in vascular tone has been attributed to defective sympathetic
and parasympathetic nervous systems6; and/or decreased responsiveness to vasoconstrictors
through altered cellular signaling transduction systems coupled with the upregulation of the nitric
oxide synthetase system.5
For elective surgical procedures, Bonfante et al7 describe managing a GS patient with preprocedure saline infusions (1.5 Liters/3 times per week) in order to overcome the chronic
hypovolemia, hypokalemia, and hypotension. The case study patient was slightly hypotensive in
the preoperative holding room: BP 97/60 mmHg. Throughout the procedure the IV fluids and
two boluses of phenylephrine 100 mcg were utilized successfully for blood pressure control. In
future GS cases, an operating room with blood tubing and fluid warmer prepared, large bore IV
access, and a colloid readily available, would be more prudent in the event of difficult blood
pressure control.
A higher prevalence of polyuria and nocturia, accentuating their decreased circulating fluid
volume8 places the GS patient at risk for developing chronic nephropathy due to acute prerenal
failure, secondary to chronic hypovolemia.7 Preservation of kidney function is further
complicated by the fasting status of surgical patients. Anesthesia practitioners need to recognize
the chronic and acute fluid volume deficits associated with GS patients. The case study patient
was managed with LR infusion according to fluid volume requirements calculated from patient
ideal body weight. A total of 1500 mL of LR was administered. Based on the evidence, it may
have been beneficial to give an additional 1500 mL of LR to compensate for the chronic
hypovolemia and NPO status of the patient. Additionally, the placement of a urinary catheter
may have been beneficial to improve intraoperative fluid volume assessment and guide fluid
management.
Hypokalemia leads to fatigue, weakness, muscle cramps, and pain. Severe manifestations of
hypokalemia can include hand and feet spasms, tetany, rhabdomyolysis, and paralysis.5 In the
2001 descriptive study by Cruz et al8 84% of the GS patients reported having some degree of
cramping, with 42% reporting frequent cramping. Patients who sought medical attention for the
musculoskeletal manifestations of GS were typically treated with intravenous potassium and/or
magnesium and started oral supplementation for prophylaxis.8
The patient in the case report was asymptomatic despite her hypokalemia: potassium level 2.9
mmol/L. After anesthetic planning and discussion the CRNA and anesthesiologist realized her
potassium level was in her normal range and did not want to increase the level because her body
41
had adapted to this hypokalemia. As discussed previously, a baseline ECG and continuous ECG
monitoring in the operating room were compared to assess for symptomatic electrolyte
disturbances needing attention during the perioperative period.
GS is one of the most common inherited renal disorders affecting patients today. An awareness
of the potential complications common in patients with GS will allow for more consistent and
precise monitoring, patient management, and delivery of anesthesia for these patients.
Anticipating and thoroughly preparing an evidence-based and patient specific anesthetic plan
will help minimize perioperative management difficulties and enhance patient safety.
References
1. Farmer JD, Vasdev GM, Martin DP. Perioperative considerations in patients with gitelman
syndrome: A case series. J Clin Anesth. 2012;24(1):14-18. doi:
10.1016/j.jclinane.2011.04.009
2. Shaer AJ. Inherited primary renal tubular hypokalemic alkalosis: A review of gitelman and
bartter syndromes. Am J Med Sci. 2001;322(6):316-332.
3. Simon DB, Karet FE, Hamdan JM, DiPietro A, Sanjad SA, Lifton RP. Bartter's syndrome,
hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the na-K-2Cl
cotransporter NKCC2. Nat Genet. 1996;13(2):183-188. doi: 10.1038/ng0696-183
4. Foglia PE, Bettinelli A, Tosetto C, et al. Cardiac work up in primary renal hypokalaemiahypomagnesaemia (gitelman syndrome). Nephrol Dial Transplant. 2004;19(6):1398-1402.
doi: 10.1093/ndt/gfh204
5. Favero M, Calo LA, Schiavon F, Punzi L. Miscellaneous non-inflammatory musculoskeletal
conditions. bartter's and gitelman's diseases. Best Pract Res Clin Rheumatol. 2011;25(5):637648. doi: 10.1016/j.berh.2011.10.013
6. Calo LA. Vascular tone control in humans: Insights from studies in bartter's/gitelman's
syndromes. Kidney Int. 2006;69(6):963-966. doi: 5000253
7. Bonfante L, Davis PA, Spinello M, et al. Chronic renal failure, end-stage renal disease, and
peritoneal dialysis in gitelman's syndrome. Am J Kidney Dis. 2001;38(1):165-168. doi:
S027263860149874X
8. Cruz DN, Shaer AJ, Bia MJ, Lifton RP, Simon DB, Yale Gitelman's and Bartter's Syndrome
Collaborative Study Group. Gitelman's syndrome revisited: An evaluation of symptoms and
health-related quality of life. Kidney Int. 2001;59(2):710-717. doi: kid540
Mentor: Kevin Buettner, CRNA, PhD
42
Anesthetic Considerations a for Patient with Cri du Chat Syndrome
Katie Carmer, BSN
Newman University
Keywords: Cri du Chat, cat cry syndrome, hypotonia, microretrognathia, airway anatomy
Also known as cat cry syndrome or 5p-syndrome, Cri du Chat is a rare genetic condition that is
caused by deletion of genetic material on the small arm (the p arm) of chromosome 5.1 The most
common manifestations usually include a high-pitched cat-like cry, mental retardation, delayed
development, distinctive facial features, small head size (microcephaly), widely-spaced eyes
(hypertelorism), low birth weight, and hypotonia.2 Of highest concern are the adverse effects on
the respiratory, cardiac systems, and neurologic systems, but the gastrointestinal,
musculoskeletal, and endocrine systems must also be evaluated judiciously prior to development
of an anesthetic plan. A detailed summary of these anesthetic implications will be discussed.
Case Study
A 14-year-old female with known Cri du Chat syndrome was scheduled for tooth extraction. The
patient weighed 35.5 kg; an accurate height was unable to be obtained due to contractures. The
patient’s medical history included Cri du Chat, severe muscle hypotonia, nonverbal, dysphagia,
percutaneous endoscopic gastrostomy tube, and gastroesophageal reflux disease. Patient’s
parents denied cardiac, pulmonary, or additional neurologic conditions. The patient had
undergone knee surgery in the past with a reported history of difficult intubation and respiratory
arrest post narcotic administration. Additionally, she had undergone bilateral myringotomy
tubes, hip joint surgery, eye surgery, and gastrostomy without complications.
Preoperative vitals were as follows; blood pressure 76/47 mm Hg, heart rate 100/min, respiratory
rate 16/min, oxygen saturation on room air 100%. No laboratory values were obtained. Lung
sounds were clear to auscultation bilaterally, and heart rate and rhythm were regular. The patient
had a very small mouth opening with a decreased thyromental distance and a Mallampati 3
classification. Hypotonia was present in the patient’s neck muscles, and she was unable to
support her head independently. After administration of midazolam 15 mg via gastric tube, a
22G IV was placed in the left antecubital region. The patient then received IV ondansetron 4 mg.
Following transport to the operating room, pulse oximetry, blood pressure cuff, and
electrocardiogram leads were placed, and the patient was preoxygenated with 10 L/min O2 for 5
minutes. Due to patient’s history of difficult intubation, video laryngoscopy and difficult airway
cart were immediately available in the operating room. General anesthesia was induced with
lidocaine 40 mg and propofol 100 mg. Mask ventilation was established without difficulty and
rocuronium 10 mg was administered. Additionally, sevoflurane was administered via face mask.
Direct laryngoscopy with a Miller 2 blade provided a grade 1 view of the patient’s vocal cords.
Placement of a 6.0 cuffed endotracheal tube was attempted unsuccessfully. Placement of a 5.5
cuffed endotracheal tube was successful with inflation of cuff provided with 0.5 ml air. The
endotracheal tube was taped at 18 cm at the lip, and there was no change in dentition or mucosa
from preoperative state. Patient was placed on pressure support ventilation to maintain tidal
43
volumes 215-240 ml until return of spontaneous ventilation.
General anesthesia was maintained with sevoflurane 1.7-2.0% end tidal concentration in O2 2
L/min. Vital signs remained stable throughout induction and no vasopressors were required
throughout the case. The oral surgeon localized the extraction sites with bupivacaine 0.25% 6
mL, and no opioid was administered throughout the case. With return of spontaneous ventilation,
patient maintained adequate tidal volumes and neuromuscular blockade was antagonized with
neostigmine 1 mg and glycopyrrolate 0.2 mg at the end of the case. The endotracheal tube was
removed after pupils were midline and patient eye opening to voice. She was monitored for
apnea in the post anesthesia care unit for 45 minutes and discharged home the same day without
need for opioid administration in recovery.
Discussion
Most cases of Cri du Chat are not inherited. Rather, the chromosomal deletion occurs as a
random event during the formation of reproductive cells or in early fetal development, and is
diagnosed at birth. The cause of this deletion is unknown and occurs in 1:15,000 to 1:50,000
births.2 People with Cri du Chat typically have no history of the condition in their family.1 In 1015% of cases, one of the parents is a carrier of a chromosomal abnormality, known as a
translocation. The parent, not showing any signs of having the syndrome itself, unknowingly
transfers the abnormality to his/her offspring. Because of this, it is recommended that parents
receive genetic testing following diagnosis of their child.
Patients with Cri du Chat have various presentations. The presence of such variations may be
related to the size of the chromosomal deletion. These patients may present with characteristic
high-pitched cry, facial abnormalities, mental and physical retardation, hypotonism,
microcephaly, microretrognathia, possible high palate, and varied neural, renal and cardiac
abnormalities.3 Most individuals with Cri du Chat syndrome have difficulty with speech and
language development, but half of these children learn sufficient verbal skills to communicate.1
Additional characteristics may include feeding difficulties, delays in walking, hyperactivity and
scoliosis. Although a small number of children are born with serious organ defects and other lifethreatening medical conditions, most individuals with Cri du Chat syndrome have a normal life
expectancy. Not all patients with Cri du Chat present with all of these symptoms, but potential
abnormalities involving airway anatomy as well as neurological, cardiac and respiratory systems
require particular assessment.
As this patient did not exhibit any cardiac or neurologic concerns, other than muscular
hypotonia, the main concern was the patient’s known difficult airway and history of respiratory
compromise following opioid administration. A thorough airway assessment was difficult to
obtain due to the patient’s inability to cooperate. Obvious visible concerns were present,
including a small recessed chin and small mouth opening. Difficult airway supplies were
immediately available in the operating room, including Glidescope, laryngeal mask airways,
bougies, multiple endotracheal tubes and laryngoscope blades, as well as emergency airway
supplies. After consultation with the surgeon, it was determined that a regular oral endotracheal
tube would be acceptable for these two extractions, avoiding nasal intubation and potential
trauma to the airway. Trauma to the airway could result in swelling and a bloody field obscuring
44
visualization and leading to laryngospasm. Elective fiberoptic intubation is another option that
could have been utilized in this situation. This could be accomplished safely with a ketamine
induction to maintain spontaneous respiration, intranasal oxymetazoline to prevent epistaxis,
nasal airway, laryngotracheal topical anesthetic for supraglottic and glottic anesthesia, and a
pediatric fiberoptic bronchoscope for visualization of the airway.4 This patient was successfully
and atraumatically intubated with direct laryngoscopy.
Gastrointestinal reflux is common in Cri du Chat patients, and general anesthesia exacerbates
weak sphincter tone at the gastroesophageal junction. Particular attention should be paid to NPO
status and home medications, with consideration then given to preoperative treatment. Rapid
sequence intubation should be utilized if indicated.
The patient’s hypotonia was taken into careful consideration. An anesthetic technique that
minimizes respiratory depression should be utilized with drugs that are short-acting and rapidly
metabolized.5 Children with neuromuscular disease will typically have an increased sensitivity to
non-depolarizing neuromuscular blocking agents. The use of a nerve stimulator and short-acting
neuromuscular blocking agents is recommended only if surgically necessary. In patients with
neuromuscular disease, succinylcholine should generally be avoided as there can be dramatic,
life-threatening increases in serum potassium, as well as an increased risk of malignant
hyperthermia and rhabdomyolysis.5 However, there is no known association with these risks in
hypotonia produced by Cri du Chat syndrome.6 Furthermore, administration of opioid decreases
patient response to hypercarbia, decreasing the respiratory drive and compromising the
respiratory system in a patient with concurrent baseline muscle weakness. Hypotonia can include
pharyngeal muscles, and patients should be observed closely for postoperative airway
obstruction.6 In this case, propofol and a small dose of rocuronium were administered to
facilitate tracheal intubation. No opioid was administered and the patient’s respirations were
supported transiently until timely return of spontaneous ventilation. Neuromuscular blockade
was antagonized at the end of the case to ensure adequate return to baseline respiratory function.
Patients with Cri du Chat can present with multisystem involvement, which almost always
include airway abnormalities. When caring for a patient with Cri du Chat syndrome, the
anesthesia practitioner must tailor the anesthetic plan to the unique needs of this population,
paying particular attention to airway concerns and muscular hypotonia.
References
1. Gu H, Jiang J, Li J, et al. A familial Cri-du-Chat/5p deletion syndrome resulted from rare
maternal complex chromosomal rearrangements (CCRs) and/or possible chromosome 5p
chromothripsis. PLoS ONE. 2013;8(10):e76985. doi:10.1371/journal.pone.0076985.
2. Mainardi PC. Review: Cri du Chat syndrome. Orphanet Journal of Rare Diseases.
2006:1(33).
3. Sweeney S. Cri du Chat syndrome: case presentation and review. Journal Of Behavioral
Optometry [serial online]. July 2012;23(4):94-98. Available from: CINAHL Complete,
Ipswich, MA. Accessed April 17, 2015.
4. Slesnick TC, Gertler R, Miller-Hance WC. Essentials of cardiology. In Coté CJ, Lerman
J, Todres ID, eds. A Practice of Anesthesia for Infants and Children. 4th ed. Philadelphia,
PA: Saunders Elsevier; 2009:293-330.
45
5. Ragoonanan V, Russell W. Anaesthesia for children with neuromuscular disease.
Continuing Education Anaesthesia Critical Care Pain. 2010;10(5):143-147. Accessed
April 17, 2015.
6. Baum VC, O’Flaherty JE. Anesthesia for Genetic, Metabolic, and Dyspmorphic
Syndromes of Childhood. 3rd ed. Philadelphia, PA: Lippincott, Williams, and Wilkins;
2015.
Mentor: Megan Ginter, CRNA, MSNA
Managing Accidental Dural Punctures with Spinal Catheters
Tyler Borne, MN
Louisiana State University Health Sciences Center
Introduction
Regional anesthesia is the most commonly used non-emergent technique in the parturient patient
population.1 It allows a safer delivery of anesthesia for both mother and baby when compared to
general anesthesia in non-emergent situations.1 However, there are still risks with this technique.
One of these risks is an accidental dural puncture (ADP). An ADP is typically encountered
during attempts to locate the epidural space when the Tuohy needle is unintentionally inserted
past the epidural space, through the dura, and into the subarachnoid space. The passage of the
Tuohy needle into the subarachnoid space produces a tear in the dura, creating a route for
cerebral spinal fluid to leak out of the spinal canal, even after the needle has been removed. The
leakage of CSF lowers intracranial pressure and is thought to be the main causative factor in the
development of postdural puncture headache (PDPH).2
While there is a multitude of available research on the treatment of PDPH, less information is
available on the prevention on PDPH following ADP. Prior to the 1990s, when an ADP
occurred, it was common practice to remove the needle and re-site the epidural.3 An alternative
method of managing an ADP by passing an epidural catheter through the needle into the
subarachnoid space was first described by Cohen et al. in 1989.3 Since the inception of this
spinal catheter technique many benefits have been noted in the literature regarding this approach,
which include; reduced rates of PDPH, a more rapid establishment of analgesia, and a lower rate
of repeat dural puncture and/or epidural catheter failure.4-7 In contrast, the literature also implies
mixed results and will require further review in order to determine firm evidence-based practice
recommendations. The purpose of this analysis is to determine if the evidence supports
utilization of a spinal catheter following ADP as best practice. Current literature was reviewed to
better understand the incidence of ADP, complications resulting from ADP, and an investigation
of the two management techniques.
Methodology
Evidence-based Analysis Model
46
The PICO format assisted in framing a clinical question into a relevant search criterion. The
PICO parameters include: P (patient population) = Parturient patients with an ADP, I (current
intervention) = placement of an epidural catheter into the subarachnoid space, C (contrasting
intervention) = removal of epidural needle and reattempting placement of an epidural catheter
into an adjacent epidural space, O (outcome of interest) = the rate of PDPH and the rate of
complications secondary to ADP management technique.
Purpose
The purpose of this evidence-based practice analysis is to examine the incidence of ADP
complications following either placement of an epidural catheter in the subarachnoid space or
reattempting epidural catheter placement into an adjacent epidural space in the laboring
parturient population.
The clinical questions that guided the literature search were: (1) In the parturient population does
the ADP management technique impact the rate of PDPH and (2) Is there a significant difference
in the rate of complications secondary to the chosen ADP management technique?
Search Models
Research articles were obtained through electronic databases such as: PubMed, EBSCO, and
OVID. The search for literature was confined between the years 2009-2014 in order to ensure the
most current information was included in this literary analysis.
Search Terms
Accidental dural puncture, inadvertent dural puncture, spinal catheter, intrathecal catheter,
epidural catheter, complications, and postdural puncture headache.
Levels of Evidence
Eleven studies were included in the evidence-based practice analysis. Of the eleven studies there
were one meta-analysis and one quantitative systematic review, both provided Level I evidence.
Three studies which produced Level II evidence, a non-randomized prospective controlled cohort
study and two retrospective cohort study. Lastly, six articles are deemed expert opinions and are
classified Level V evidence.
Literature Analysis
The incidence of ADP during epidural placement has a range of 0.19% to 3.6% in the obstetric
population, but is found to be as high as 6.6% in one study.5,8 The incidence of PDPH following
ADP with an epidural needle has been found to range from 52% to 88%.2 PDPH is a serious
complication of ADP because symptoms can be severe enough to prevent the mother from caring
for her newborn, increase length of hospital stay, and relate to a possible increase in morbidity
and mortality in the obstetric population.8 Serious complications resulting from an ADP include:
postural headache, orthostatic hypotension, diplopia, tinnitus, dizziness, neck pain, myalgia,
nausea, vomiting, and subdural hematoma.2,4 Typically, PDPH “symptoms develop within 48
hours and may be delayed up to five days”.4 (p3) “Generally, there is gradual improvement in the
symptoms with time. Seventy percent tend to resolve within one week, 95% within six weeks,
and 96% within six months”.4 (p3)
47
Common practice for the management of an ADP is to remove the epidural needle and to
reattempt insertion of the epidural needle at an adjacent vertebral interspace. Reattempting
epidural placement in a patient that has already experienced an ADP carries a 9% risk of another
ADP.7 Laboring anesthesia can be administered through the spinal catheter allowing for a more
rapid progression of regional anesthesia, which negates the need for a second epidural
attempt.5,7,9 Both ADP management techniques carry a risk for complications; however, the
literature demonstrates the rate of complications to be three times greater in the epidural re-site
group compared to the spinal catheter group.9 The literature also demonstrates that a spinal
catheter results in a reduction in the rate of PDPH, although conflicting data on this topic is
present in the current literature. In an effort to provide the most current evidenced-based practice
recommendations, six articles with research data were reviewed. The results are summarized in
Table 1.
Table 1. Recent literature regarding PDPH rates and neuraxial complications
Articles
Description
Results
Apfel,
Saxena,
Cakmakkay,
Gaiser,
George, and
Radke,
20108
Quantitative systematic review
Short-term spinal catheter versus re-siting epidural:
Spinal catheter: 145 total ADP, 90 PDPH (62% PDPH rate)
Epidural re-site: 161 total ADP, 124 PDPH (77% PDPH rate)
Prevention of postdural puncture
headache after accidental
dural puncture
Test for overall effect: Z=0.99 (P = 0.32)
Long-term spinal catheter versus re-siting epidural:
Spinal catheter: 104 total ADP, 32 PDPH (30% PDPH rate)
Epidural re-site: 214 total ADP, 123 PDPH (57% PDPH rate)
Test for overall effect: Z=1.20 (P=0.23)
Reduction of PDPH was not significant in the short-term or
long-term spinal catheter group
Heesen,
Klöhr,
Rossaint,
Walters,
Straube,
Van de
Velde, 20135
Russell,
20126
Meta-analysis
Spinal catheter: 469 total ADP, 258 PDPH (55% PDPH rate)
Epidural re-site: 470 total ADP, 310 PDPH (65% PDPH rate)
Insertion of an intrathecal
catheter following accidental
dural puncture
Test for overall effect: Z = 1.85 (P = 0.06)
Prospective controlled study
The incidence of PDPH headache was reduced but not to a rate
that concluded significant results.
Spinal catheter: 50 total ADP, 36 PDPH (72% PDPH rate)
Epidural re-site: 47 total ADP, 29 PDPH (62% PDPH rate)
(P = 0.2)
Continuous spinal analgesia
versus repeat epidural analgesia
after accidental dural puncture in
labor
PDPH were demonstrated to be higher in the spinal catheter
group compared to the re-site epidural group. The difference in
the PDPH could not conclude significant results
Risk of another ADP with reattempting epidural placement was
demonstrated to be 9 %
Participants in the repeat epidural group suffered complications
at a rate three times greater than those in the spinal catheter
48
Van de
Velde,
Schepers,
Berends,
Vandermeer
sch, De
Buck, 20097
Retrospective cohort study
Ten years of experience with
accidental dural puncture and
post-dural puncture headache in
a tertiary obstetric anesthesia
department
group
Spinal catheter: 27 total ADP, 14 PDPH (52% PDPH rate)
Epidural re-site: 28 total ADP, 17 PDPH (61% PDPH rate)
(P > 0.05)
Review of literature:
Spinal catheter: 317 total ADP, 161 PDPH (51% PDPH rate)
Epidural re-site: 282 total ADP, 187 PDPH (66% PDPH rate)
Chi2 = 14.8; P < 0.001
Significant results concluded that spinal catheters reduce the
rate of PDPH. However, “most trials or case series were nonrandomised, unblinded or of insufficient power to detect a
difference”9 (p334)
Rahim,
Ranasinghe,
Moaveni,
CohnHochman,
201311
Retrospective cohort study
Spinal catheter: 761 total ADP, 312 PDPH (40.9% PDPH rate)
Complications of Continuous
Intrathecal Catheters in Obstetric
Patients
Overall failure rate of spinal catheters was 5.9%, 45 of the 761
inserted spinal catheters
Four patients in the spinal catheter group requiring intubation
and ventilation resulting from a high block
There were no reported cases of meningitis, arachnoiditis,
cauda equina syndrome or epidural hematoma
Silva and
Halpern,
201010
Expert Opinion review of
literature
Complications of neuraxial
analgesia
Complication
Epidural
Failure rate
14%
Dural puncture
0.21%-1.6%
Nerve damage cause 0.6:100,000
by needle trauma
Epidural abscess 3 per 100,000
Meningitis
0–3.5:100.000
Epidural hematoma 1:168,000
CSE
_
10%
0.20%-1.7%
3.9:100,000
?
0–3.5:100,000
?
PDPH Prevention
The two main neuraxial regional techniques utilized in the parturient population involve the
delivery of anesthesia either into the epidural space or into the spinal canal. Both techniques
carry an inherent risk for PDPH. Since the 1960s, there has been a bounty of literature on the
prevention of PDPH with the administration of spinal anesthesia, termed a subarachnoid block.
However, until recently, literature has been limited on interventions that can be utilized to reduce
the rate of PDPH following ADP with an epidural needle. In 1989, a technique was published
involving passing an epidural catheter into the subarachnoid space and dosing this catheter in
increments appropriate for a spinal dose in order to provide laboring analgesia.3 In this case
study all 10 patients obtained appropriate relief from labor pain, but what Cohen et al. also noted
was that only two of his 10 patients developed a PDPH.3 With the spinal catheter technique, a
20% rate of PDPH following ADP was demonstrated, which was found to be much lower than
the national average of 52 to 88% with re-siting the epidural.2,3 While the evidence from this
study appears convincing, a control group and power analysis are not included and therefore the
impact on current practice is not clear.3
49
Cohen et al’s study was the first to examine the spinal catheter as an intervention following
ADP, while it lacked the ability to independently change current practice at that time, it did
create a foundation for research. Apfel et al. and Hessen et al. each performed a meta-analyses to
determine if a spinal catheter demonstrated a reduced rate of PDPH when compared to re-siting
the epidural.5,8 Use of the spinal catheter technique did not demonstrate a statistical difference in
the prevention of PDPH, with a RR of 0.88 (95% CI 0.68–1.14, P < 0.32) for PDPH for shortterm spinal catheterization and a RR of 0.21 (95% CI 0.02–2.65,P < 0.23) for long-term spinal
catheterization, defined as a period longer than 24 hr.5,8 Van de Velde et al. performed a
prospective non-randomized control trial and concluded similar results as the two previous
studies, with spinal catheters showing no clear benefit on PDPH rates.7 “When data from
obstetric reports are combined, prolonged intrathecal catheter placement significantly reduces the
risk of PDPH after ADP to 51% compared with 66% in those who have the catheter re-sited
epidurally (Chi2 = 14.8: P < 0.001)”. 7 (p334) It was noted in this study that most trials in the
review of literature were non-randomized, the researcher was not blinded to data collection, or
the trial was of inadequate power to detect a difference.9 One conclusion that was universally
agreed upon is that spinal catheter placement following ADP is a promising intervention for
preventing PDPH and that a large, multi-center, prospective, randomized, blinded trial is needed
to clarify this issue.5-8
Decreased rate of complications with spinal catheters
Russell performed a prospective controlled study of continuous spinal analgesia versus repeat
epidural analgesia after accidental dural puncture in labor, and what was demonstrated in this
study was an increased rate of complications when the epidural was reattempted following an
ADP.6 The risk of another ADP with reattempting epidural placement was demonstrated to be 9
%; this was in line with other previous studies.6,9 In fact, it was noted in this study that
participants in the repeat epidural group suffered complications at a rate three times greater than
those in the spinal catheter group.9 Common complications encountered in each study include:
multiple repeat ADP, ineffective analgesia when the epidural is placed on subsequent attempts,
epidural catheter failure, total spinal block, and epidural vein puncture with a subsequent high
block.6,9 In addition, the use of a spinal catheter was not without its complications in this study,
including spinal catheter failure, failure due to paresthesia, failure to pass spinal catheter, and a
total spinal.6
In a retrospective quality assurance study, 12,590 regional anesthetic procedures for labor
analgesia were reviewed, in this study it was noted that 14% (P < 0.001) of inserted epidurals
failed.10 In this trial, 5.6% of the epidural catheters placed had to be removed and replaced,
despite functioning initially upon insertion.10 While this study does not offer a comparative data
analysis due to the fact that spinal catheters were not specifically addressed, it should be noted
inadequate analgesia with the epidural catheter alone was reported at 8.4% while the combined
single shot spinal-epidural (CSE) group reported 4.2%.10 One can deduce that incorporation of
spinal anesthesia improved patient analgesia compared to the use of the epidural as the sole route
of delivery.9
Rahim et al performed a retrospective cohort study examining the rate of spinal catheter
complications following ADP.11 A total of 761 patients had spinal catheters placed during the
50
study period, and of the 761 catheters placed, 45 failed (5.9%).11 The other complication noted
was that four patients had respiratory problems resulting from a high block and required
intubation.11 These findings indicate spinal catheters have a relatively low rate of failure when
compared to epidural catheters, 5.9% compared to 14%. When anesthesia personnel cause an
ADP after having difficulty finding the epidural space, it appears more beneficial to place a
spinal catheter and provide a route for rapid anesthesia rather than to place the patient at risk for
further complications with re-siting the epidural.6,9,11
Despite the literature available to support spinal catheter use, recent surveys have found that only
25 to 36% of ADPs are managed with spinal catheter insertion.2 Accidental misuse and
infections were the most common listed reason for not placing a spinal catheter and opting to resite the epidural. The fear of misuse is that anesthesia personnel would dose the spinal catheter as
though it were in the epidural space, which could be fatal. There is potential for this problem in
that the catheters look identical in appearance; however, this can be easily managed with firm
adherence to clear policies and protocols.2 Infection is the other concern anesthesia personnel list
as a reason for abstaining from the insertion of a spinal catheter following ADP. The main issue
is that spinal catheters present a direct connection to the central nervous system, which could
potentially increase the risk of developing meningitis. In review of the literature, only one
retrospective cohort study was present, yet this study involving 761 parturient patients with
spinal catheters did not observe any incidences of meningitis or arachnoiditis .11 However, there
is a larger pool of data available on epidural, single shot spinal, and CSE infection rates that give
potential insight into the rate of infection with neuraxial techniques in the parturient population.10
Silva and Halpern reviewed the findings of 10 surveys and found the incidence of epidural
abscess to be 0.2-3.7 per 100,000 obstetric epidurals. Similar results were obtained concerning
bacterial meningitis following spinal anesthesia, 0-3.5 per 100,000 (95% CI).10 One would
conclude that this risk for infection is very low regardless of the neuraxial technique. However,
further research is warranted to confirm a similar rate of infection in relation to spinal catheters
and the other neuraxial techniques in practice.
Conclusion
There is conflicting evidence in the literature regarding the effectiveness of spinal catheters
providing a decreased risk of PDPH. Considering that ADP has a demonstrated PDPH incidence
of 52 to 88% in the obstetric population, prophylactic interventions need to be considered.2,8
PDPH symptoms can be severe enough to prevent the mother from caring for her newborn,
increase length of hospital stay, and relate to a possible increase in morbidity and mortality in the
obstetric population.8 It would therefore appear to be more sensible to enact preemptive
interventions aimed at preventing the onset of PDPH rather than starting treatment after the
clinical presentation.8 Anesthesia professionals must be sure that these preemptive interventions
are not responsible for further increasing morbidity and mortality.5 More research in the form of
a large, well-designed, double-blind, randomized controlled multicenter trial is necessary in
order to draw more definitive conclusions in regards to spinal catheters impact on the incidence
of PDPH following ADP.5-8
Present literature on the incidence of complications following an ADP illustrates a pattern of
decreased risk with the utilization of the spinal catheter technique.6-8 Studies by Hessen et al.,
51
Russell, Gaiser, and Van de Velde et al. suggest that when the anesthesia personnel has had
difficulty identifying the epidural space prior to an ADP, introduction of a spinal catheter greatly
reduces the risk of complications stemming from re-siting the epidural, mainly a repeat ADP and
catheter failure.5,6,9,11 The spinal catheter technique is optimal because it relieves the patient of
potential suffering through another epidural or a repeat ADP.6,9 Lastly, the spinal catheter
technique allows for the anesthesia personnel to provide a more rapid and highly successful
anesthetic in comparison to re-siting the epidural.2,4-7 Based on these benefits, change in current
practice should be directed toward introduction of a spinal catheter following an ADP,
particularly if prior identification of the epidural space was difficult.
References
1. Ashok J. Complications of regional and general anaesthesia in obstetric practice. Indian J
Anaesth. 2010;54(5):415-420.
2. Nath G, Subrahmanyam M. Headache in the parturient: pathophysiology and management of
post-dural puncture headache. Journal of obstetric anaesthesia and critical care.
2011;1(2):55-66.
3. Cohen S, Daitch JS, Goldiner PL. An alternative method for management of accidental dural
puncture for labor and delivery. Anesthesiology. 1989;70(1):164-165.
4. Sagadai, S. Mini topic review: postdural puncture headache. NHS evidence – surgery,
anaesthesia, perioperative, and critical care. 2010:1-11.
http://files.sld.cu/anestesiologia/files/2012/08/postdural_headache_mtr.pdf
5. Heesen M, Klohr S, Rossaint R, Walters M, Straube S, Van de Veldec M. Insertion of an
intrathecal catheter following accidental dural puncture: a meta-analysis. Int J Obstet Anesth.
2013;22:26-30.
6. Russell IF. A prospective controlled study of continuous spinal analgesia versus repeat
epidural analgesia after accidental dural puncture in labour. Int J Obstet Anesth. 2012;21:716.
7. Van de Velde M, Schepers R, Berends N, Vandermeersch E, De Buck F.Ten years of
experience with accidental dural puncture and post-dural puncture headache in a tertiary
obstetric anaesthesia department. Int J Obstet Anesth. 2009;17:329-335.
8. Apfel CC, Saxena A, Cakmakkaya OS, Gaiser R, George E, Radke O. Prevention of
postdural puncture headache after accidental dural puncture: a quantitative systematic
review. Br J Anaesth. 2010; 105(3):255-263.
9. Gaiser RR. Postdural puncture headache: a headache for the patient and a headache for the
anesthesiologist. Curr Opin Anaesthesiol. 2013; 26(3):296-303.
10. Silva M, Halpern SH. Epidural analgesia for labor: current techniques. Local and Regional
Anesthesia. 2010;3:143–153.
11. Rahim MA, Ranasinghe JS, Moaveni DA, Cohn-Hochman J. Complications of Continuous
Intrathecal Catheters in Obstetric Patients. Society for Obstetric Anesthesia and Perinatology
Web site. http://soap.org/display_2013_abstract.php?id=O1%206 Published 2013. Accessed
February 29, 2014.
Mentor: Laura S. Bonanno, CRNA, DNP
52
Editorial
I am always excited when I receive a submission from a nurse anesthesia program that has never
submitted before. Newman University has their first (of many, I hope) report published in this
issue. Since I assumed the role of Editor the number of programs represented on the board has
almost doubled, and the number of individuals serving on the board has more than doubled!
On that note, I am also very pleased to welcome two new members of the Editorial Board:
Johanna Newman, CRNA , DNAP - Florida International University
Bryan Tune, CRNA, DNP - National University
As always, I am grateful for all of the hard work and time contributed by the volunteers for this
journal!
Sincerely,
Vicki C. Coopmans, CRNA, PhD
Editor
“The International Student Journal of Nurse Anesthesia is produced
exclusively for publishing the work of nurse anesthesia students. It is
intended to be basic and introductory in its content. Its goal is to introduce
the student to the world of writing for publication; to improve the practice of
nurse anesthesia and the safety of the patients entrusted to our care.”
To access prior issues of the ISJNA visit the following link:
www.aana.com/studentjournal
53
INTERNATIONAL STUDENT JOURNAL OF NURSE ANESTHESIA
GUIDE FOR AUTHORS
MISSION STATEMENT
The International Student Journal of Nurse Anesthesia is produced exclusively for publishing the work of nurse
anesthesia students. It is intended to be basic and introductory in its content. Its goal is to introduce the student to
the world of writing for publication; to improve the practice of nurse anesthesia and the safety of the patients
entrusted to our care.
ITEMS ACCEPTED FOR PUBLICATION
Case reports, research abstracts, evidence-based practice (EBP) analysis reports, and letters to the editor may be
submitted. These items must be authored by a student under the guidance of an anesthesia practitioner mentor
(CRNA or physician). The mentor must submit the item for the student and serve as the contact person during the
review process. Items submitted to this journal should not be under consideration with another journal. We
encourage authors and mentors to critically evaluate the topic and the quality of the writing. If the topic and the
written presentation are beyond the introductory publication level we strongly suggest that the article be submitted
to a more prestigious publication such as the AANA Journal.
ITEM PREPARATION & SUBMISSION
Student authors prepare case reports, abstracts, EBP analysis reports, and letters to the editor with the guidance of a
mentor. Only students may be authors. Case and EBP analysis reports must be single-authored. Abstracts may have
multiple authors. Mentors should take an active role in reviewing the item to ensure appropriate content, writing
style, and format prior to submission.
The original intent of this journal was to publish items while the author is still a student. In order to consistently
meet this goal, all submissions must be received by the editor at least 3 months prior to the author’s date of
graduation.
PEER REVIEW
Items submitted for publication are initially reviewed by the editor. Items may be rejected, or returned to the mentor
with instructions for the author to revise and resubmit prior to initiation of the formal review process. All accepted
submissions undergo a formal process of blind review by at least two ISJNA reviewers. After review, items may be
accepted without revision, accepted with revision, or rejected with comments.
General guidelines
1. Items for publication must adhere to the American Medical Association Manual of Style (AMA, the same guide
utilized by the AANA Journal and such prominent textbooks as Nurse Anesthesia by Nagelhout and Plaus). The
review process will not be initiated on reports submitted with incorrect formatting and will be returned to the
mentor for revision. Please note the following:
a. Use of abbreviations is detailed in Section 14. Spell out acronyms/initialisms when first used. If you are
using the phrase once, do not list the acronym/initialism at all.
b. Instructions regarding units of measure can be found in Section 18. In most cases The International System
of Units (SI) is used. Abbreviations for units of measure do not need to be spelled out with first use. Some
examples: height/length should be reported in cm, weight in kg, temperature in oC, pressure in mm Hg or
cm H20.
c. In general, first use of pulmonary/respiratory abbreviations should be expanded, with the following
exceptions: O2, CO2, PCO2, PaCO2, PO2, PaO2. Please use SpO2 for oxygen saturation as measured by
pulse oximetry.
d. Use the nonproprietary (generic) name of drugs - avoid proprietary (brand) names. Type generic names in
lowercase. When discussing dosages state the name of the drug, then the dosage (midazolam 2 mg).
e. Use of descriptive terms for equipment and devices is preferred. If the use of a proprietary name is
necessary (for clarity, or if more than one type is being discussed), give the name followed by the
manufacturer and location in parenthesis:
“A GlideScope (Verathon Inc., Bothell, WA) was used to . . . .”
Please note, TM and ® symbols are not used per the AMA manual.
f. Examples of referencing are included later in this guide.
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2.
3.
4.
5.
6.
7.
8.
9.
Report appropriate infusion rates and gas flow rates:
a. When reporting infusion rates report them as mcg/kg/min or mg/kg/min. In some cases it may be
appropriate to report dose or quantity/hr (i.e. insulin, hyperalimentation). If a mixture of drugs is being
infused give the concentration of each drug and report the infusion rate in ml/min.
b. Keep the gas laws in mind when reporting flow rates. Report the liter flows of oxygen and nitrous oxide
and the percent of the volatile agent added to the gas mixture. Statements such as “40% oxygen, 60%
nitrous oxide and 3% sevoflurane” do not = 100% and are thus incorrect. For example, “General anesthesia
was maintained with sevoflurane 3% inspired concentration in a mixture of oxygen 1 L/min and air 1
L/min”.
Only Microsoft Word file formats will be accepted with the following criteria:
a. Font - 12 point, Times New Roman
b. Single-spacing (except where indicated), paragraphs separated with a double space (do not indent)
c. One-inch margins
d. Place one space after the last punctuation of sentences. End the sentence with the period before placing the
superscript number for the reference.
e. Do not use columns, bolds (except where indicated), or unconventional lettering styles or fonts.
f. Do not use endnote/footnote formats.
Do not use Endnotes or similar referencing software. Please remove all hyperlinks within the text.
Avoid jargon.
a. ‘The patient was reversed’ - Did you physically turn the patient around and point him in the opposite
direction? “Neuromuscular blockade was antagonized.”
b. The patient was put on oxygen. "Oxygen was administered by face mask."
c. The patient was intubated and put on a ventilator. “The trachea was intubated and respiration was
controlled by a mechanical ventilator.
d. The patient had been on Motrin for three days. “The patient had taken ibuprofen for three days.”
e. Avoid the term “MAC” when referring to a sedation technique - the term sedation (light, moderate, heavy,
unconscious) sedation may be used. Since all anesthesia administration is monitored, the editors prefer to
use specific pharmacology terminology rather than reimbursement terminology.
Use the words “anesthesia professionals” or “anesthesia practitioners” when discussing all persons who
administer anesthesia (avoid the reimbursement term “anesthesia practitioners”)
References
a. Again, the AMA Manual of Style must be adhered to for reference formatting.
b. All should be within the past 8 years, except for seminal works essential to the topic being presented.
c. Primary sources are preferred.
d. All items cited must be from peer-reviewed sources – use of internet sources must be carefully considered
in this regard.
e. Numbering should be positioned at the one-inch margin – text should begin at 1.25”.
See each item for additional information.
Heading for each item (Case Report, Abstract, EBPA Report) must adhere to the following format:
Title (bold, centered, 70 characters or less)
[space]
Author Name (centered, include academic credentials only)
Name of Nurse Anesthesia Program (centered)
[space]
Anticipated date of graduation (italics, centered, will be removed prior to publication)
E-mail address (italics, centered, will be removed prior to publication)
[space, left-justify from this point forward]
Keywords: (‘Keywords:’ in bold, followed by keywords (normal font) that can be used to identify the report in an
internet search.)
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Case Reports
The student author must have had a significant role in the conduct of the case. The total word count should be
between 1200 – 1400 words. References do not count against the word count. Case reports with greater than 1400
words will be returned to the mentor for revision prior to initiation of the review process. The following template
demonstrates the required format for case report submission.
Heading (see #9 above in General Guidelines)
[space]
A brief introductory paragraph of less than 100 words to focus the reader’s attention. This may include historical
background, demographics or epidemiology (with appropriate references) of the problem about to be discussed. It is
written in the present tense. Although it is introductory, the heading word ‘Introduction’ is not used. Be certain to
cite references in this section, especially statistics and demographics pertaining to your topic.
[space]
Case Report (bold, 400-500 words)
[space]
This portion discusses the case performed in 400 words or less, and is written in the past tense. Do not justify
actions or behaviors in this section; simply report the events as they unfolded. Present the case in an orderly
sequence. Some aspects need considerable elaboration and others only a cursory mention.
Patient description: height, weight, age, gender.
History of present illness
Statement of co-existing conditions/diseases
Mention the current medications, generic names only. (Give dosage and schedule only if that information is
pertinent to the consequences of the case.)
Significant laboratory values, x-rays or other diagnostic testing pertinent to the case. Give the units after the
values (eg. Mmol/L or mg/dL).
Physical examination/Pre-anesthesia evaluation - significant findings only. Include the ASA Physical Status
and Mallampati Classification only if pertinent to the case.
Anesthetic management (patient preparation, induction, maintenance, emergence, post-operative recovery).
Despite the detail presented here it is only to help the author organize the structure of the report. Under most
circumstances if findings/actions are normal or not contributory to the case then they should not be described.
Events significant to the focus of the report should be discussed in greater detail. The purpose of the case report is to
set the stage (and ‘hook’ the reader) for the real point of your paper which is the discussion and teaching/learning
derived from the case.
[space]
Discussion (bold, 600-800 words)
[space]
Describe the anesthesia implications of the focus of the case report citing current literature. Describe the rationale
for your actions and risk/benefits of any options you may have had. This section is not merely a pathophysiology
review that can be found in textbooks. Relate the anesthesia literature with the conduct of your case noting how and
why your case was the same or different from what is known in the literature. Photographs are discouraged unless
they are essential to the article. Photos with identifiable persons must have a signed consent by the person
photographed forwarded to the editor via first class mail. Diag must have permission from original author. This is
the most important part of the article. In terms of space and word count this should be longer than the case
presentation. End the discussion with a summary lesson you learned from the case, perhaps what you would do
differently if you had it to do over again.
[space]
References (bold)
[space]
A minimum of 5 references is recommended, with a maximum of 8 allowed. No more than 2 textbooks may be
included in the reference list, and all references should be no older than 8 years, except for seminal works essential to
the topic. This is also an exercise in evaluating and using current literature.
[space]
Mentor: (bold, followed by mentor name and credentials in normal text)
E-mail address (italics, will be removed prior to publication)
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Research Abstracts
Research abstracts are limited to 500 words. References are not desired but may be included if considered essential.
Note that this abstract is different from a research proposal. This abstract reports the outcome of your study. Use the
same format described for the case report with the exception of the section headings:
Heading (see #9 above in General Guidelines)
[space]
Introduction (bold)
[space]
A brief introductory paragraph including purpose and hypotheses.
[space]
Methods (bold)
[space]
Include research design and statistical analyses used
[space]
Results (bold)
[space]
Present results – do not justify or discuss here.
[space]
Discussion (bold)
[space]
Discuss results
[space]
References (bold)
[space]
Not required, but a maximum of 5 references is allowed.
[space]
Mentor: (bold, followed by mentor name and credentials in normal text)
E-mail address (italics, will be removed prior to publication)
EBP Analysis Reports
Evidence-based practice analysis reports are limited to 3000 words. Please do not include an abstract. The report
should provide a critical evaluation of a practice pattern in the form of a clinical question about a specific intervention
and population. The manuscript should:
1. Articulate the practice issue and generate a concise question for evidence-based analysis. A focused
foreground question following either the PICO or SPICE format should be used.
2. Describe the methods of inquiry used in compiling the data.
3. Critically analyze the quality of research reviewed and applicability to different practice settings.
4. Draw logical conclusions regarding appropriate translation of research into practice.
The same general format guidelines apply with the exception of the section headings as below. Please note that text
books and non-peer reviewed internet sources should be avoided, and sources of reference should be less than 8
years old unless they are seminal works specifically related to your topic of inquiry:
Heading (see #9 above in General Guidelines)
[space]
Introduction (bold)
[space]
Briefly introduce the reader to the practice issue or controversy, describe the scope or significance or problem, and
identify the purpose of your analysis. Describe the theoretical, conceptual, or scientific framework that supports your
inquiry.
[space]
Methodology (bold)
[space]
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Include the format used for formulating the specific question you seek to answer, search terms and methods used, and
levels of evidence.
[space]
Literature Analysis (bold)
[space]
Review and critique the pertinent and current literature, determining scientific credibility and limitations of studies
reviewed. Your synthesis table would be included in this section. Your review and discussion of the literature should
logically lead to support a practice recommendation. Subheadings may be used if desired.
[space]
Conclusions (bold)
[space]
Summarize the salient points that support the practice recommendation and make research-supported recommendations
that should improve the practice issue, while also acknowledging any limitations or weaknesses
[space]
References [bold]
[space]
A minimum of 8 references is recommended, with a maximum of 12 allowed.
Letters to the Editor
Students may write letters to the editor topics of interest to other students. Topics may include comments on
previously published articles in this journal. Personally offensive, degrading or insulting letters will not be accepted.
Suggested alternative approaches to anesthesia management and constructive criticisms are welcome.
The length of the letters should not exceed 100 words and must identify the student author and anesthesia program.
AMA MANUAL OF STYLE
The following is brief introduction to the AMA Manual of Style reference format along with some links to basic,
helpful guides on the internet. The website for the text is http://www.amamanualofstyle.com/oso/public/index.html.
It is likely your institution’s library has a copy on reserve.
http://www.docstyles.com/amastat.htm#Top
http://healthlinks.washington.edu/hsl/styleguides/ama.html
Journal names should be in italics and abbreviated according to the listing in the PubMed Journals Database. The
first URL below provides a tutorial on looking up correct abbreviations for journal titles; the second is a link to the
PubMed where you can perform a search.
http://www.nlm.nih.gov/bsd/viewlet/search/journal/journal.html
http://www.ncbi.nlm.nih.gov/pubmed
The International Student Journal of Nurse Anesthesia (ISJNA) is not listed in the PubMed Database. For the
purpose of citing the ISJNA in this Journal use “Int Student J Nurse Anesth” as the abbreviation. The titles of text
books are also printed in italics. Please pay close attention to ensure correct punctuation.
Journals
Note there is a comma after the first initials until the last author, which has a period. If there are six or less authors
cite all six. If there are more than six authors cite only the first three followed by “et al.” Only the first word of the
title of the article is capitalized. The first letters of the major words of the journal title are capitalized. There is no
space between the year, volume number, issue number, and page numbers. If there is no volume or issue number,
use the month. If there is an issue number but no volume number use only the issue number (in parentheses). The
pages are inclusive - do not omit digits.
Some journals (and books) may be available both as hard copies and online. When referencing a journal that has
been accessed online, the DOI (digital object identifier) or PMID (PubMed identification number) should be
included (see example below).
Journal, 6 or fewer authors:
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Hamdan A, Sibai A, Rameh C, Kanazeh G. Short-term effects of endotracheal intubation on voice. J Voice.
2007;21(6):762-768.
Journal, more than 6 authors:
Chen C, Nguyen MD, Bar-Meir E, et al. Effects of vasopressor administration on the outcomes of microsurgical
breast reconstruction. Ann Plast Surg. 2010;65(1):28-31. PMID: 20548236.
Texts
There is a difference in citing a text with one or more authors from a text with one or more editors. Texts that are
edited give credit to the authors of the chapters. They must be annotated and the inclusive pages of the chapter are
noted. Texts that are authored do not have different chapter authors, the chapter is not cited by heading but the
inclusive pages where the information was found are cited, unless the entire book is cited.
Text:
Stoelting R, Dierdorf S. Anesthesia and Co-Existing Disease. 3rd ed. Philadelphia: Churchill Livingstone;
1993:351-354.
Chapter from a text:
Burkard J, Olson RL, Vacchiano CA. Regional anesthesia. In Nagelhout JJ, Plaus KL, eds. Nurse Anesthesia. 4th ed.
St. Louis:Elsevier; 2010:977-1030
Each chapter was written by a different author. Note the chapter’s author gets the prominent location. The chapter
title is cited; “editor” is abbreviated in a lowercase. The word “edition” is also abbreviated and in lower case. The
inclusive pages of the chapter are cited.
Electronic references
Only established, peer-reviewed sources may be referenced. Please do not reference brochures or informational
websites where a peer-review process cannot be confirmed. Authors are cautioned to not copy and paste from these
without full credit and quotation marks where appropriate. Electronic references are cited using the following
format:
Author (or if no author, the name of the organization responsible for the site). Title. Name of journal or website.
Year;vol(issue no.):inclusive pages. doi: or URL. Published [date]. Updated [date]. Accessed [date].
For online journals, the accessed date may be the only date available, and in some cases no page numbers.
Examples:
Kamangar N, McDonnell MS. Pulmonary embolism. eMedicine. http://www.emedicine.com/med/topic1958.htm.
Updated August 25, 2009. Accessed September 9, 2009.
Gupta A, Aggarwal N, Sharma D. Ultrasound guided ilioinguinal block. The Internet Journal of Anesthesiology.
2011;29(1).
http://www.ispub.com/journal/the_internet_journal_of_anesthesiology/volume_29_number_1/article/ultrasoundguided-ilioinguinal-block.html. Accessed August 1, 2011.
ACADEMIC INTEGRITY
Issues of academic integrity are the primary responsibility of the author and mentor. Accurate and appropriate
acknowledgement of sources is expected. Any violation will be cause for rejection of the article.
“Plagiarism is defined as the act of passing off as one's own the ideas, writings, or statements of another. Any act of
plagiarism is a serious breach of academic standards, and is considered an offense against the University subject to
disciplinary action. Any quotation from another source, whether written, spoken, or electronic, must be bound by
quotation marks and properly cited. Any paraphrase (a recapitulation of another source's statement or idea in one's
own words) or summary (a more concise restatement of another's ideas) must be properly cited.”
http://grad.georgetown.edu/pages/reg_7.cfm
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HOW TO SUBMIT AN ITEM
Manuscripts must be submitted by the mentor of the student author via e-mail to [email protected] as an
attachment. The subject line of the e-mail should be “Submission to Student Journal”. The item should be saved in
the following format – two-three word descriptor of the article_author’s last name_school abbreviation_mentor’s
last name_date (e.g. PedsPain_Smyth_GU_Pearson_5.19.09)
REVIEW AND PUBLICATION
If the editor does not acknowledge receipt of the item within one week, assume that it was not received and please
inquire. Upon receipt, the Editor will review the submission for compliance with the Guide to Authors. If proper
format has not been following the item will be returned to the mentor for correction. This is very important as all
reviewers serve on a volunteer basis. Their time should be spent ensuring appropriate content, not making format
corrections. It is the mentor’s responsibility to ensure formatting guidelines have been followed prior to submission.
Once the item has been accepted for review the Editor will send a blinded copy to a Section Editor, who will then
coordinate a blinded review by two reviewers who are not affiliated with the originating program. The reviewers
recommend publication to the Section Editor or make recommendations for changes to be addressed by the author.
The Section Editor will return the item to the Editor, who will return it to the mentor for appropriate action (revision,
approval to print). If the article is returned to the author for repair it is usually to answer a specific question related
to the case that was not clear in the narrative or it asks the author to provide a reference for a statement. Every effort
is made to place the returned article in the earliest next issue.
The goal is for all articles submitted by students to be published while the author is still a student. Therefore,
deadlines must be met and the entire process must be efficient. If an item is not ready for publication within 3
months after the student author has graduated it will no longer be eligible for publication. For this reason it is
recommended that case reports be submitted at least 4-6 months prior to the student author’s anticipated graduation
date.
Mentors of the papers may be asked to serve as reviewers of case reports by student authors from other prog and will
be listed as contributing editors for the issue in which the item is published.
PHOTOS
Photos of students for the front cover of the Journal are welcome. Include a legend describing the activity and who is
in the photo and identify the photographer. Only digital photos of high quality will be accepted via email to
[email protected]. There must be a follow up hard copy signed by all present in the photo, as well as the
photographer/ owner of the original photo, giving consent to publish the photo. Mail that consent to:
Vicki C. Coopmans, CRNA, PhD
Webster University
470 E. Lockwood Ave. Suite 15
St. Louis, MO 63119
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SUBMISSION CHECK LIST
___ AMA Manual of Style and other format instructions are adhered to.
___ Total word count not exceeded (1400 for case report, 500 for abstract, 3000 for EBPA).
___ The item is one continuous Word document without artificially created page breaks.
___ Verbatim phrases and sentences are quoted and referenced.
___ All matters that are not common knowledge to the author are referenced.
___ Generic names for drugs and products are used throughout and spelled correctly in lower-case.
___ Units are designated for all dosages, physical findings, and laboratory results.
___ Endnotes, footnotes not used.
___ Jargon is absent.
Heading
___ Concise title less than 70 characters long
___ Author name, credentials, nurse anesthesia program, graduation date and email are included.
___ Five Keywords are provided
Case Report
___ Introduction is less than 100 words.
___ Case Report section states only those facts vital to the account (no opinions or rationale)
___ Case report section is 400-500 words and not longer than the discussion.
___ Discussion section is 600-800 words.
___ Discussion of the case management is based on a review of current literature
___ Discussion concludes with lessons learned and how the case might be better managed in the future.
Abstract
___ The 500 word count maximum is not exceeded.
___ Abstract reports the outcome of your study.
___ Includes Introduction, Methods, Results, and Conclusion sections.
EBPA Report
___ The 3000 word count maximum is not exceeded.
___ A critical evaluation of a practice pattern in the form of a precise clinical question about a specific intervention and
population is presented.
___ A focused foreground question following either the PICO or SPICE format is used.
___ Includes Introduction, Methodology, Literature Analysis, and Conclusion sections.
References
___ AMA Style for referencing is used correctly.
___ Reference numbers are sequenced beginning with one and superscripted.
___ References are from anesthesia and other current primary source literature.
___ All inclusive pages are cited, texts as well as journals.
___ Journal titles are abbreviated as they appear in the PubMed Journals Database.
___ Number of references adheres to specific item guidelines.
___ Internet sources are currently accessible, reputable, and peer reviewed.
Transmission
___ The article is sent as a attachment to [email protected]
___ The file name is correctly formatted (e.g. PedsPain_Smyth_GU_Pearson_5.19.09)
___ It is submitted by the mentor with cc to the student author
___ The words "Submission to Student Journal" are in the subject heading.
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